There is evidence that calcium (Ca) physiology is altered in essential hypertension. Intracellular Ca ions have direct effect on peripheral vascular tone, and hypertensive have increased intracellular free Ca that decreases to normal levels with antihypertensive treatment. Serum Ca levels have also been negatively associated with 24-hour urine Na and positively associated with potassium (K) excretion. Blaustein (1977) suggested that intracellular Ca increase in hypertension is due to altered Na-Ca exchange across the cellular membrane of smooth muscles. Altered sodium (Na) transport in red blood cells (RBC) of hypertensives is seen by some researchers as a useful tool for detecting predisposition to, and differentiating essential from secondary hypertension. However, attempts to associate dietary Na and RBC Na transport have ben disappointing. Similarly, potassium (KC1) supplementation has been associated with BP lowering and KC1 deficiency is associated with RBC Na excursion, but there is no evidence that KC1 supplementation changes RBC Na transport, and, to date, KC1 deficiency experiments have not reliably increased BP. If abnormal caution transport is in fact a marker and a precursor of hypertension it is important to identify potentially modifiable environmental or life style variable that might possibly be useful for positive purposes. Three experiments, using SHR and WKY rats, are proposed to investigate if a) dietary CA affects RBC Na transport b) Ca and Na interact to influence RBC Na transport, c) Ca and K interact to influence RBC Na transport. In Exp. I, the rats will be placed on digest of high, normal or low Ca. In Exp. II, they will be placed on combination diets of high and low Ca and Na. In Exp. III, they will be placed on combination diets of high and low Ca and K. The rats will be maintained on the diets for eight weeks following which blood will be collected via heart puncture for RBC Na flux analyses. Eight weekly tail cuf BP will be collected to compare with the Na flux data.

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