Altered cation transport in non-insulin-dependent diabetic hypertension

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Abstract
Erythrocyte cation transport and intracellular calcium in 15 black type II diabetic hypertensives were compared with 11 otherwise similar non-diabetic hypertensives and 16 normal black adults. The diabetic hypertensives were then randomized into either a placebo group or a calcium-supplemented (600 mg/day) group and studied again after 4 weeks. Na+,K+-ATPase activity was significantly lower in both groups of hypertensives than in the normotensives. In contrast, Ca-ATPase activity was similar among the non-diabetic hypertensive and normotensives but was markedly (approximately 60%) suppressed in the diabetics, while intracellular calcium was proportionally elevated. Calcium supplements significantly increased Ca-ATPase activity and reduced intracellular calcium and blood pressure compared with the placebo group. We conclude that type II diabetes is characterized by a defect in Ca-ATPase which may be responsible for increases in intracellular calcium and vascular resistance and which is partially corrected by dietary calcium supplementation.

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