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Step I Magnesium and parathyroid
Started by Miracoli
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Hypomagnesemia stimulates PTH secretion and hypermagnesemia inhibits PTH secretion.
However, severe hypomagnesemia decreases PTH secretion since Mg2+ is a co-factor for adenyl cyclase generating cAMP which is required for PTH storage, activation and secretion.
However, severe hypomagnesemia decreases PTH secretion since Mg2+ is a co-factor for adenyl cyclase generating cAMP which is required for PTH storage, activation and secretion.
Yes. In most tissues, high Ca intracellular favors exocytosis but in chief cells of parathyroid gland, high Ca intracellular inhibits exocytosis of PTH while low Ca intracellular and high cAMP favors exocytosis of PTH. Mg2+ is a co-factor for adenyl cyclase.
the "Mg2+ is a co-factor for adenyl cyclase" explains for the "severe hypomagnesemia decreases PTH secretion" but what is the mechanism for "Hypomagnesemia stimulates PTH secretion and hypermagnesemia inhibits PTH secretion"?
the "Mg2+ is a co-factor for adenyl cyclase" explains for the "severe hypomagnesemia decreases PTH secretion" but what is the mechanism for "Hypomagnesemia stimulates PTH secretion and hypermagnesemia inhibits PTH secretion"?
Simple feedback mechanism.
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Of course.
Hypocalcemia stimulates PTH secretion and hypercalcemia inhibits PTH secretion through the CaSR.
How about "Hypomagnesemia stimulates PTH secretion and hypermagnesemia inhibits PTH secretion"? What is the mechanism for this feedback control?
Exactly the same i.e. via the CaSR.
That's what we were recently taught.
really? i thought in the chief cells where pth is released, magnesium takes over the role of calcium, in which calcium normally causes exocytosis of substances from cells(but in the chief cells magnesium causes exocytosis), thus no magnesium, no exocytosis- no PTH?
"Cao2+ is not the only CaSR agonist. A variety of divalent (e.g., Mg2+ and Sr2+) and trivalent (La3+ and Gd3+) cations activate the receptor, as do highly positively charged organic molecules, such as the polyamines (i.e., spermine), aminoglycoside antibiotics (e.g., neomycin), protamine, and polyarginine (21, 152). These polycationic agonists are termed type 1 agonists, and they activate the receptor even without extracellular Ca2+ being present."
Source:
Am J Physiol Renal Physiol. 2010 Mar; 298(3): F485–F499.
Published online 2009 Nov 18. doi: 10.1152/ajprenal.00608.2009
PMCID: PMC2838589
Physiology and pathophysiology of the calcium-sensing receptor in the kidney
okay, so how does a moderate decrease in magnesium increase PTH release?
Although calcium is the major agonist (and thus activator) of the CaSR, magnesium also plays a clinically significant role as an agonist too. Moderate decreases of magnesium leads to more inactivated CaSR -> inactivated CaSR leads to increased PTH release
is the CaSR location only in the PTH cells?
