Calcium Metabolism in Experimental Hypertension

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Abstract
Clearly, Ca2+ metabolism is altered in hypertension at both the whole animal and cellular level. Furthermore, dietary Ca2+ deficiency is associated with human hypertension at the epidemiologic level and oral Ca2+ supplementation lowers blood pressure in human and experimental hypertension. In this review, we have presented the integrated view that a constellation of systemic abnormalities of Ca2+ metabolism in hypertension results in inefficient Ca2+ conservation and relative Ca2+ deficiency. Furthermore, the cellular findings in hypertension suggest increased cell membrane Ca2+ permeability and a compromised ability of the cell to remove or sequester intracellular Ca2+. Paradoxically this leads to increased intracellular free Ca2+ stores in the face of reduced extracellular Ca2+. Unfortunately most of the whole animal and cellular work has been carried out using different tissues. Nonetheless, it seems reasonable to hypothesize that abnormal Ca2+ handling at the cellular level is ultimately reflected at the organ and whole animal level so that alterations in vascular smooth muscle, intestine, kidney, erythrocytes, and so on are due to the same underlying defect manifested in many cell lines. The underlying defect may involve the cell membrane Ca2+-ATPase (68), an intrinsic membrane binding protein (114), a cell membrane Ca2+ channel, or perhaps some other process.

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