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Altered cation transport in non-insulin-dependent diabetic hypertension: effects of dietary calcium
M B Zemel1, B A Bedford, P C Zemel
1Division of Endocrinology, Metabolism and Hypertension, Wayne State University, Detroit, Michigan 48202.
Insights
Type II diabetes in hypertensive individuals shows suppressed calcium pump (Ca-ATPase) activity, leading to higher intracellular calcium. Calcium supplements improved this function and lowered blood pressure.
Area of Science:
- Biochemistry
- Cardiovascular Physiology
- Endocrinology
Background:
- Hypertension and type II diabetes are significant public health concerns.
- Erythrocyte cation transport is implicated in blood pressure regulation.
- Intracellular calcium levels play a crucial role in vascular smooth muscle contraction.
Purpose of the Study:
- To investigate erythrocyte cation transport and intracellular calcium in black patients with type II diabetes and hypertension.
- To determine the effect of calcium supplementation on these parameters.
Main Methods:
- Comparison of erythrocyte Na+,K+-ATPase and Ca-ATPase activity, and intracellular calcium levels.
- Randomized controlled trial of calcium supplementation (600 mg/day) versus placebo in diabetic hypertensives.
- Blood pressure measurements before and after intervention.
Main Results:
- Diabetic hypertensives exhibited significantly suppressed Ca-ATPase activity and elevated intracellular calcium compared to non-diabetic hypertensives and normotensive controls.
- Na+,K+-ATPase activity was lower in both hypertensive groups.
- Calcium supplementation increased Ca-ATPase activity, reduced intracellular calcium, and lowered blood pressure in diabetic hypertensives compared to placebo.
Conclusions:
- Type II diabetes is associated with a Ca-ATPase defect in erythrocytes, contributing to increased intracellular calcium and potentially vascular resistance.
- Dietary calcium supplementation can partially correct this defect and improve blood pressure in diabetic hypertensives.
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.