Describe the action of calcium and vitamin D on the parathyroid gland.
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Rania Mahmoud
Action of calcium and vitamin D on parathyroid gland
– They have the calciumsensing receptor (CaSR) and the vitamin D receptor
– The CaSR detects small decreases in extracellular calcium concentrations and increases the release of stored PTH in seconds or minutes.
– If the calcium drop lasts for an extended period of time (hours, days), PTH production rises at the post-transcriptional stage, altering the stability of the mRNA.
– Variations in the nature of VDRAs and their receptors can result in various effects and a synergistic effect on parathyroid cells.
– PTH mRNA degradation is reduced when serum calcium levels fall.
– Calcitriol binds to VDR and inhibits the transcription of the PTH gene and the production of this hormone.
Action of calcium and vitamin D on parathyroid gland
Calcium interacts with PTH via its calcium sensing receptor(CaSR) which is G protein coupled membrane receptor. CaSR detects small changes in calcium and if calcium is low in ECF then there is release of Preformed PTH in seconds and minutes. if ECF calcium remains low for hours or days then there is increased in PTH which occurs at post transcriptional level of PTH mRNA. for example decrease in calcium decrease degradation of PTH mRNA. opposite happens if ecf caclium is high
Vitamin D
Vitamin D interacts with PTH via Vitamin D Receptor and acts as transcriptor factor by reducing pth synthesis unlike calcium
Calcium
Ca is sensed by Ca sensing receptors (CaSR), the latter detects minute changes in serum calcium, this initiate series of intracellular event leading to release of already formed PTH (inside vesicles), and also leads to increase in synthesis of more PTH if stimulation persists more than minutes, by increasing transcription of mRNA of PTH
Vitamin D
Vitamin D binds to parathyroid via Vitamin D Receptor (VDR).
Vitamin D acts as a typical “Steroid hormone”, so binding of vitamin D to VDR initiate intracellular signal that goes to Nucleus to increase transcription of PTH gene to mRNA then translation to PTH
In CKD, prolongation of the above stimulants leads to diffuse hyperplasia of Parathyroid gland, and further prolongation leads to Nodular hyperplasia
Action of calcium and vitamin D on parathyroid Gland
*Parathyroid gland has CaSR and VDR
*S.Ca has inverse relation with PTH (low Ca stimulate PTH release then synthesis then stability relative to time of exposure to hypocalcemia,, similarly increased S.Ca has negative feedback on PTH.
* vitamin D has inverse relation with PTH secretion ( vitamin D deficiency stimulate PTH secretion)
The action of calcium and vitamin D on the parathyroid gland first of all Calcium in the ECF binds to CaSR in the parathyroid cells which leads the increase in intercellular calcium ,this leads to reduction of PTH release.
hypocalcemia leads to low of intercellular calcium and increase of PTH.
PTH increases renal calcium reabsorption ,osteoclast bone resorption,increase of FGF23 release.PTH stimulates renal coverting of (25[OH]D) to 1,25(OH)2D, which increase intestinal calcium absorption.
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors, the calcium- sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release. If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
In advanced stages of CKD-MBD, and as a consequence of the decrease in calcium and calcitriol and the increase in phosphate, the parathyroid gland is subjected to a permanent proliferative stimulus that triggers severe forms of secondary hyper- parathyroidism with hyperplasia of the gland, first diffuse and then nodular, with a significant reduction in the CaSR, VDR and FGFR/Klotho expression which ends in a poor response of the parathyroid glands to calcium, VDR activators (VDRA) and FGF23.
CA and vit. D act on parathyroid gland via CASR and vit DR
Hypocalcemia increase production of PTH
decrease calcitriol sensitize VDR and secretion of pth
vis versa increase calcidoil or calcetriod suppress pth
Thanks Dr. Elsayed.
Here is a more clarified answer:
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
When calcium is high the CaSR lead to the degradation of PTH; the opposite is applicable when in the case of hypocalcemia.
Vitamin D acts on PTH via VDR receptors. vitamin D either in calcidiol or calcitriol form, suppresses the transcription of PTH and prevent its increase
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Ca act on parathyroid gland via ca senseing receptor and vit d act on vit d specific receptor if ca level decrease causing stimulation to increase secrearion of pth also decrease level of vit d causing stimulation of secretion on the other hand if increase level of calciterol or ca causing inhibiton of pth
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Calcium and vit D exert their actions on the parathyroid cells through their specific receptors, the calcium sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively. CaSR is a G protein-coupled membrane receptor, while VDR is a nuclear receptor that, when bound to its activator (any active form of active vitamin D (VDRA), acts as a transcription factor. Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells. The CaSR detects small decreases in extracellular calcium concentrations, rapidly increases the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release. If calcium decrease persists for longer periods, the synthesis of PTH increases, reduces the degradation of PTH increasing its stability and half-life; the increase in calcium has the opposite effect .
Due to the previously discussed changes lead to stimulation of the parathyroid gland so expected in CKD 5 high prevalence of secondary hyperparathyroidism with high bone turnover, but nowadays due to several factors, such as excess intaake of calcium and vitamin D in the recent decades the more frequent pattern of bone lesions has changed from high to low bone turnover In advanced stages of CKD as the parathyroid gland is subjected to a continues stimulus causing parathyroid nodule, result in significant reduction in the CaSR, VDR which ends in a poor response of the parathyroid glands to calcium, vit D analogues and FGF23.
Thanks Dr. Elsayed
Here is a more clarified answer:
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors, the calcium sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
-changes in calcium levels affect parathyroid gland by acting on calcium sensing receptors (CaSRs) as hypocalcemia cause upregulation of these receptors and stimulate parathyroid gland to release the preformed vesicles then increase synthesis by acting on mRNA and post transcriptional level to compensate hypocalcemia and vice versa in hypercalcemia
-as regard vit D defiency , it stimulate PTH release and action and PTH stimlate active vit D to compensate also for hypocalcemia in CKD patients in contrast to the action of FGF-23
1-Calcium works through its receptor on the parathyroid gland CaSR functions on parathyroid glands:
-PTH synthesis, PTH secretion, and parathyroid cellular proliferation.
-CaSR senses the circulating levels of Ca2+ and translates this information via a complex of signaling pathways either to inhibit or stimulate secretion of PTH by chief cells of the parathyroid gland. Low serum Ca2+ levels inhibit the CaSR so that PTH is secreted whereas high levels of Ca2+ activate the CaSR and inhibit PTH.
2-Calcitriol inhibit both the secretion and synthesis of PTH .
Calcium is a major regulator of PTH secretion. Minute changes in the s.calcium are detected by a specific membrane CaSR (highly expressed on the parathyroid gland). The CaSR tightly regulates changes in PTH secretion in response to serum calcium.  A decrease in s.Ca results in the release of stored PTH in seconds or mins.
Persistently low s.Ca levels lead to a direct increase in PTH mRNA concentrations via posttranscriptional actions and stimulate the proliferation of parathyroid cells over days or weeks.
Calcitriol normally acts on the VDR in the parathyroid gland to suppress PTH transcription but not PTH secretion.
1-Calcium work through its receptor on the parathyroid gland CaSR functions on parathyroid glands:
-PTH synthesis, PTH secretion, and parathyroid cellular proliferation.
-CaSR senses the circulating levels of Ca2+ and translates this information via a complex of signaling pathways either to inhibit or stimulate secretion of PTH by chief cells of the parathyroid gland. Low serum Ca2+ levels inhibit the CaSR so that PTH is secreted whereas high levels of Ca2+ activate the CaSR and inhibit PTH.
2-Calcitriol inhibit both the secretion and synthesis of PTH
Describe the action of calcium and vitamin D on the parathyroid gland.
the parathyroid glands have sensing receptors for both calcium and Vit. D.
both calcium and Vit.D do an inhibitory action on parathyroid glands.
therefore, hypocalcemia and Vit. D deficiency do upregulation of their corresponding receptors on parathyroid glands and inducing hyperplasia and finally adenoma, resulting in 2ry hyperparathyroidism
in late stages, autonomus secretion of PTH will occur resulting in tertiary hyperparathyroidism.
excess calcium and /or Vit. D do the opposite effect on parathyroid glands with resulting adynamic bone disease.
Thanks Dr. Ibrahim:
Here is a more clarified answer:
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
When s. Calcium decrease the CasR will be stimulated and within seconds to minutes there will be secretion of stored PTH, if this low level of s. Ca persist for hours or days the synthesis of PTH increase in the posttranscriptional level changing the stability of mRNA, the low calcium level will decrease the degradation of PTHmRNA and so increase its stability and half life and vice versa occurs when s. Ca increase
The calcitriol binds to VDR in the PT gland it will decrease the transcription of PTH gene and reduce the secretion of the hormone.
As the renal function reduce the control of minerals metabolism become difficult and phosphate increases and calcitriol decrease.
In advanced kidney failure with decrease in Calcium and calcitriol and increase phosphorus there will be PT gland proliferation which is polyclonal at the beginning then monoclonal proliferation with decrease CasR, VDRA and FGFR/klotho there will be decrease response to Calcium, calcitriol and FGF23.
Could you describe the action of calcium and vitamin D on the parathyroid gland?
Calcium works on PTH gland via CaSR
CaSR senses the circulating level of ca and whether to inhibit or increase PTH secretion.
Hypocalcemia will stimulate PTH secretion, while hypercalcemia will inhibit PTH secretion. Very important to know that CaSR is activated in case of high CA, which will reduce PTH secretion and vice versa.
In regards to VitD :
it will inhibit both secretion and synthesis as well
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
-Describe the action of calcium and vitamin D on the parathyroid gland?
Calcium effect is through its receptor on the parathyroid gland called CaSR; A G-protein coupled membrane receptor. Hypocalcemia stimulate PTH production(decrease degradation of prolonged PTH half-life) and hypercalcemia suppress PTH release. phosphate acts in the same way(through CaSR) but in the opposite direction.
Vitamin D effect is through its receptor on the parathyroid gland known as VDRA; a nuclear receptors which acts as a transcription factor upon bind to vitamin D(= the activator). Calcitriol bind to its receptor(VDRA) and suppress PTH by decreasing its transcription & synthesis.
The action of calcium and vitamin D on the parathyroid gland
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors
CaSR: detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH and vice versa. If hypocalcemia persists for longer periods, PTH increases post-transcriptionally by modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
VDRA: calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors, the calcium- sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
CaSR is a G protein-coupled membrane receptor, while VDR is a nuclear receptor that, when bound to its activator (any active form of active vitamin D (VDRA), acts as a transcription factor.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release.
In persistent hypocalcemia, the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Low Calcium will stimulate CaSR on Parathyroid gland and these will cause increasing the PTH secretion.
The mechanism is through exocytosis of already made PTH if acute need.
Or increase of stability of mRNA if chronic(days).
High calcium will decrease PTH secretion through inhibition of CaSR.
It will cause more degeneration of mRNA PTH (post transcriptional)
There is VDR receptor on nucleous of parathyroid Cells which after binding to Vitamin D causes reduction in transcription of the PTH Gene and the synthesis of PTH.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Calcium and calcitriol act on para-thyroid cells through their receptors, the CaSR and VDR, respectively. VDR is a nuclear receptor that operates as a transcription factor when attached to any active form of vitamin D (VDRA). CaSR is a G-protein-coupled membrane receptor. VDRAs and receptors may operate differently and synergistically on parathyroid cells.
The CaSR detects minor drops in extracellular calcium concentrations and releases stored PTH within seconds or minutes. If the stimulus is reversed, it suppresses hormone release. PTH production rises post-transcriptionally if calcium decreases for hours or days, affecting mRNA stability. The reduction in serum calcium increases PTH mRNA stability and half-life, whereas the rise decreases it.
The hormone calcitriol binds to the vitamin D receptor, which in turn allows it to exercise its action by lowering both the transcription of the PTH gene and the production of this hormone.
The action of calcium and vitD on parathyroid gland: The action of calcium: The calcium act on parathyroid gland via CaSR, the receptor through which any changes in the serum calcium level has been detected. With hypocalcemia a stored PTH has been released as a result of CaSR activation, the opposite will occur if hypercalcemia occur. The effects of vitD on parathyroid gland: VitD act on parathyroid gland via VDR which lead to downregulation of the receptor and lead to inhibit PTH release, via reduce the PTH synthesis
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Action of calcium and vitamin D on parathyroid gland
– They have the calciumsensing receptor (CaSR) and the vitamin D receptor
– The CaSR detects small decreases in extracellular calcium concentrations and increases the release of stored PTH in seconds or minutes.
– If the calcium drop lasts for an extended period of time (hours, days), PTH production rises at the post-transcriptional stage, altering the stability of the mRNA.
– Variations in the nature of VDRAs and their receptors can result in various effects and a synergistic effect on parathyroid cells.
– PTH mRNA degradation is reduced when serum calcium levels fall.
– Calcitriol binds to VDR and inhibits the transcription of the PTH gene and the production of this hormone.
Action of calcium and vitamin D on parathyroid gland
Calcium interacts with PTH via its calcium sensing receptor(CaSR) which is G protein coupled membrane receptor. CaSR detects small changes in calcium and if calcium is low in ECF then there is release of Preformed PTH in seconds and minutes. if ECF calcium remains low for hours or days then there is increased in PTH which occurs at post transcriptional level of PTH mRNA. for example decrease in calcium decrease degradation of PTH mRNA. opposite happens if ecf caclium is high
Vitamin D
Vitamin D interacts with PTH via Vitamin D Receptor and acts as transcriptor factor by reducing pth synthesis unlike calcium
Calcium
Ca is sensed by Ca sensing receptors (CaSR), the latter detects minute changes in serum calcium, this initiate series of intracellular event leading to release of already formed PTH (inside vesicles), and also leads to increase in synthesis of more PTH if stimulation persists more than minutes, by increasing transcription of mRNA of PTH
Vitamin D
Vitamin D binds to parathyroid via Vitamin D Receptor (VDR).
Vitamin D acts as a typical “Steroid hormone”, so binding of vitamin D to VDR initiate intracellular signal that goes to Nucleus to increase transcription of PTH gene to mRNA then translation to PTH
In CKD, prolongation of the above stimulants leads to diffuse hyperplasia of Parathyroid gland, and further prolongation leads to Nodular hyperplasia
Action of calcium and vitamin D on parathyroid Gland
*Parathyroid gland has CaSR and VDR
*S.Ca has inverse relation with PTH (low Ca stimulate PTH release then synthesis then stability relative to time of exposure to hypocalcemia,, similarly increased S.Ca has negative feedback on PTH.
* vitamin D has inverse relation with PTH secretion ( vitamin D deficiency stimulate PTH secretion)
The action of calcium and vitamin D on the parathyroid gland first of all Calcium in the ECF binds to CaSR in the parathyroid cells which leads the increase in intercellular calcium ,this leads to reduction of PTH release.
hypocalcemia leads to low of intercellular calcium and increase of PTH.
PTH increases renal calcium reabsorption ,osteoclast bone resorption,increase of FGF23 release.PTH stimulates renal coverting of (25[OH]D) to 1,25(OH)2D, which increase intestinal calcium absorption.
BOTH have specific receptors on the parathyroid
calcium sensing receptor (CaSR) and vit D receptor (VDR)
a. release of stored PTH at first
b. synthesis of PTH hormone at posttranscriptional level
c. decrease degradation and increase stability of PTH
vit D via it action on VDR receptor inhibit transcription of vit D synthesis
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors, the calcium- sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release. If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
In advanced stages of CKD-MBD, and as a consequence of the decrease in calcium and calcitriol and the increase in phosphate, the parathyroid gland is subjected to a permanent proliferative stimulus that triggers severe forms of secondary hyper- parathyroidism with hyperplasia of the gland, first diffuse and then nodular, with a significant reduction in the CaSR, VDR and FGFR/Klotho expression which ends in a poor response of the parathyroid glands to calcium, VDR activators (VDRA) and FGF23.
Great Dr. Asmaa
CA and vit. D act on parathyroid gland via CASR and vit DR
Hypocalcemia increase production of PTH
decrease calcitriol sensitize VDR and secretion of pth
vis versa increase calcidoil or calcetriod suppress pth
Thanks Dr. Elsayed.
Here is a more clarified answer:
When calcium is high the CaSR lead to the degradation of PTH; the opposite is applicable when in the case of hypocalcemia.
Vitamin D acts on PTH via VDR receptors. vitamin D either in calcidiol or calcitriol form, suppresses the transcription of PTH and prevent its increase
Thanks Dr. Mahmud
Ca act on parathyroid gland via ca senseing receptor and vit d act on vit d specific receptor if ca level decrease causing stimulation to increase secrearion of pth also decrease level of vit d causing stimulation of secretion on the other hand if increase level of calciterol or ca causing inhibiton of pth
Thanks Dr. Rabab
Calcium and vit D exert their actions on the parathyroid cells through their specific receptors, the calcium sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
CaSR is a G protein-coupled membrane receptor, while VDR is a nuclear receptor that, when bound to its activator (any active form of active vitamin D (VDRA), acts as a transcription factor.
Differences in the nature of the VDRAs and their receptors can induce different actions and a synergistic effect on the parathyroid cells.
The CaSR detects small decreases in extracellular calcium concentrations, rapidly increases the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release.
If calcium decrease persists for longer periods, the synthesis of PTH increases, reduces the degradation of PTH increasing its stability and half-life; the increase in calcium has the opposite effect .
Due to the previously discussed changes lead to stimulation of the parathyroid gland so expected in CKD 5 high prevalence of secondary hyperparathyroidism with high bone turnover, but nowadays due to several factors, such as excess intaake of calcium and vitamin D in the recent decades the more frequent pattern of bone lesions has changed from high to low bone turnover
In advanced stages of CKD as the parathyroid gland is subjected to a continues stimulus causing parathyroid nodule, result in significant reduction in the CaSR, VDR which ends in a poor response of the parathyroid glands to calcium, vit D analogues and FGF23.
Excellent Dr. Rola
the action of calcium and vitamin D on the parathyroid gland.hypocalcemia and decrease 1-alf hydroxylase
synthetizing and increase production of PTH
Thanks Dr. Elsayed
Here is a more clarified answer:
ACTION OF CALCIUM AND VITAMIN D ON Parathroid gland :
they exert their actions through their specific receptors (CaSR .,VDR)
IF CALCIUM DECREASE >>the synthesis of PTH increases
calcitriol bind to VDR and exerts its effect by reducing the trnscription of the PTH gene and the synthesis of this hormone
Thanks Dr. Emad
In addition:
-changes in calcium levels affect parathyroid gland by acting on calcium sensing receptors (CaSRs) as hypocalcemia cause upregulation of these receptors and stimulate parathyroid gland to release the preformed vesicles then increase synthesis by acting on mRNA and post transcriptional level to compensate hypocalcemia and vice versa in hypercalcemia
-as regard vit D defiency , it stimulate PTH release and action and PTH stimlate active vit D to compensate also for hypocalcemia in CKD patients in contrast to the action of FGF-23
Great answer Dr. Mark
1-Calcium works through its receptor on the parathyroid gland CaSR functions on parathyroid glands:
-PTH synthesis, PTH secretion, and parathyroid cellular proliferation.
-CaSR senses the circulating levels of Ca2+ and translates this information via a complex of signaling pathways either to inhibit or stimulate secretion of PTH by chief cells of the parathyroid gland. Low serum Ca2+ levels inhibit the CaSR so that PTH is secreted whereas high levels of Ca2+ activate the CaSR and inhibit PTH.
2-Calcitriol inhibit both the secretion and synthesis of PTH .
Good job Dr. Ahmed
Calcium is a major regulator of PTH secretion. Minute changes in the s.calcium are detected by a specific membrane CaSR (highly expressed on the parathyroid gland). The CaSR tightly regulates changes in PTH secretion in response to serum calcium.

A decrease in s.Ca results in the release of stored PTH in seconds or mins.
Persistently low s.Ca levels lead to a direct increase in PTH mRNA concentrations via posttranscriptional actions and stimulate the proliferation of parathyroid cells over days or weeks.
Calcitriol normally acts on the VDR in the parathyroid gland to suppress PTH transcription but not PTH secretion.
Great Dr. Amna
1-Calcium work through its receptor on the parathyroid gland CaSR functions on parathyroid glands:
-PTH synthesis, PTH secretion, and parathyroid cellular proliferation.
-CaSR senses the circulating levels of Ca2+ and translates this information via a complex of signaling pathways either to inhibit or stimulate secretion of PTH by chief cells of the parathyroid gland. Low serum Ca2+ levels inhibit the CaSR so that PTH is secreted whereas high levels of Ca2+ activate the CaSR and inhibit PTH.
2-Calcitriol inhibit both the secretion and synthesis of PTH
Great Dr. Mahmoud
Describe the action of calcium and vitamin D on the parathyroid gland.
Thanks Dr. Ibrahim:
Here is a more clarified answer:
When s. Calcium decrease the CasR will be stimulated and within seconds to minutes there will be secretion of stored PTH, if this low level of s. Ca persist for hours or days the synthesis of PTH increase in the posttranscriptional level changing the stability of mRNA, the low calcium level will decrease the degradation of PTHmRNA and so increase its stability and half life and vice versa occurs when s. Ca increase
The calcitriol binds to VDR in the PT gland it will decrease the transcription of PTH gene and reduce the secretion of the hormone.
As the renal function reduce the control of minerals metabolism become difficult and phosphate increases and calcitriol decrease.
In advanced kidney failure with decrease in Calcium and calcitriol and increase phosphorus there will be PT gland proliferation which is polyclonal at the beginning then monoclonal proliferation with decrease CasR, VDRA and FGFR/klotho there will be decrease response to Calcium, calcitriol and FGF23.
Great Dr. Israa
Could you describe the action of calcium and vitamin D on the parathyroid gland?
Calcium works on PTH gland via CaSR
CaSR senses the circulating level of ca and whether to inhibit or increase PTH secretion.
Hypocalcemia will stimulate PTH secretion, while hypercalcemia will inhibit PTH secretion. Very important to know that CaSR is activated in case of high CA, which will reduce PTH secretion and vice versa.
In regards to VitD :
it will inhibit both secretion and synthesis as well
Thanks Dr. Rihab
Here is a more clarified answer:
Describe the action of calcium and vitamin D on the parathyroid gland
vit D :
Thanks Dr. Ashraf
In addition:
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH. In cases of hypercalcemia, it reduces the hormone release.
If the calcium decrease persists for longer periods (hours, days), the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Unlike calcium, calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
-Describe the action of calcium and vitamin D on the parathyroid gland?
Great answer. Thanks Dr. Ben
wlcm prof
The action of calcium and vitamin D on the parathyroid gland
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors
CaSR: detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH and vice versa. If hypocalcemia persists for longer periods, PTH increases post-transcriptionally by modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
VDRA: calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Great answer. Thanks Dr. Mohammed
Calcium and calcitriol exert their actions on the parathyroid cells through their specific receptors, the calcium- sensing receptor (CaSR), and the vitamin D receptor (VDR), respectively.
CaSR is a G protein-coupled membrane receptor, while VDR is a nuclear receptor that, when bound to its activator (any active form of active vitamin D (VDRA), acts as a transcription factor.
The CaSR detects small decreases in extracellular calcium concentrations, increasing in seconds or minutes the release of stored PTH, if the stimulus is the opposite, it reduces the hormone release.
In persistent hypocalcemia, the synthesis of PTH increases, this occurs at the post-transcriptional level, modifying the stability of the mRNA. Whereas the decrease in serum calcium reduces the degradation of PTH mRNA, increasing its stability and half-life; the increase in calcium has the opposite effect.
Calcitriol binds to VDR and exerts its effect by reducing the transcription of the PTH gene and the synthesis of this hormone.
Excellent Dr. Alaa
Low Calcium will stimulate CaSR on Parathyroid gland and these will cause increasing the PTH secretion.
The mechanism is through exocytosis of already made PTH if acute need.
Or increase of stability of mRNA if chronic(days).
High calcium will decrease PTH secretion through inhibition of CaSR.
It will cause more degeneration of mRNA PTH (post transcriptional)
There is VDR receptor on nucleous of parathyroid Cells which after binding to Vitamin D causes reduction in transcription of the PTH Gene and the synthesis of PTH.
Good Dr. Nour
In addition:
Calcium and calcitriol act on para-thyroid cells through their receptors, the CaSR and VDR, respectively. VDR is a nuclear receptor that operates as a transcription factor when attached to any active form of vitamin D (VDRA). CaSR is a G-protein-coupled membrane receptor. VDRAs and receptors may operate differently and synergistically on parathyroid cells.
The CaSR detects minor drops in extracellular calcium concentrations and releases stored PTH within seconds or minutes. If the stimulus is reversed, it suppresses hormone release. PTH production rises post-transcriptionally if calcium decreases for hours or days, affecting mRNA stability. The reduction in serum calcium increases PTH mRNA stability and half-life, whereas the rise decreases it.
The hormone calcitriol binds to the vitamin D receptor, which in turn allows it to exercise its action by lowering both the transcription of the PTH gene and the production of this hormone.
Great Dr. Weam
The action of calcium and vitD on parathyroid gland:
The action of calcium:
The calcium act on parathyroid gland via CaSR, the receptor through which any changes in the serum calcium level has been detected.
With hypocalcemia a stored PTH has been released as a result of CaSR activation, the opposite will occur if hypercalcemia occur.
The effects of vitD on parathyroid gland:
VitD act on parathyroid gland via VDR which lead to downregulation of the receptor and lead to inhibit PTH release, via reduce the PTH synthesis
Good answer Dr. Kamal
In addition: