Constant release secretion of adrenaline and cortisol.
Activation of the Na+/Ca2+ exchanger in the distal tubule is the most likely mechanism of thiazide hypercalcemia
Thiazide-hypercalcemia is a well-known clinical condition. By inhibiting the thiazide-sensitive NaCl transporter in the distal convoluted tubule, which is closely related to calcium transport, thiazides cause an increase in sodium excretion.
Thiazides hypercalcemia decreases urine calcium levels while raising blood calcium levels via promoting calcium reabsorption from the luminal membrane into the interstitium in exchange for sodium. High calcium levels are a well-known adverse effect of thiazide hypercalcemia diuretics including hydrochlorothiazide (Microzide) and chlorthalidone, which are used to treat high blood pressure. By blocking calcium from being discharged in the urine, which can also result in kidney stones, these drugs can boost calcium levels.
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Answer:
Peer pressure from friends and others to try it, and the bandwagon effect trying to convince them to do the drug
Her hypothalamus responds by producing more hormones that maintain growth, adrenal, and thyroid function, sex hormones. it also makes ACTH or adrenocorticotropin to help make the adrenal glands work.
