Key points are not available for this paper at this time.
Design
Review
Calcium dysregulation may shape hypertension mechanisms; leaves open clinical translation pending targeted trials.
Recent developments in our knowledge of cellular calcium metabolism are reviewed. Changes in the Ca2+ concentration in the cell cytosol are a nearly universal means of coupling stimulus with response in both neural and endocrine cells. In particular, Ca2+ serves as an important intracellular messenger in the regulation of cardiac and smooth muscle function, the regulation of aldosterone secretion by K+ and angiotensin II, and the secretion of renin. Several points about the messenger role of Ca2+ are emphasized: small changes in Ca2+ concentration bring about large changes in cell response; the regulation of calcium fluxes across the plasma membrane are critical to proper cell function; and excessive calcium is a cellular toxin. An attempt is made to integrate our knowledge of the function and properties of intracellular Ca2+ receptor proteins with our knowledge of cellular calcium homeostasis, and relate this to the pathogenesis of hypertension.
No takes yet. Share an insight, caveat, or question.
Howard Rasmussen (1983) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: