Higher Na+???H+ exchange rate and more alkaline intracellular pH set-point in essential hypertension: effects of protein kinase modulation in platelets

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Abstract
Na+–H+exchange is known to be elevated in essential hypertension. To examine the mechanism of this elevation, we studied a group of 19 male hypertensive patients (mean age 46 years; systolic/diastolic blood pressure 144/99 mmHg), without medication for at least 2 weeks, and a control group of 19 male normotensives (mean age 49 years; systolic/diastolic blood pressure 118/77 mmHg). Na+–H+ exchange and intracellular pH set-point, at which the exchange is approximately nil, were studied spectroflurometrically in blood platelets loaded with 2',7'-bis carboxyethyl-5,6-carboxyfluorescein in an isotonic medium containing 60mmol/l sodium propionate, pH7.35. The exchange rate (pH per 9s at intracellular pH7.0) of hypertensives (0.050 ± 0.005) is significantly greater (P7< 0.001) than the rate of normotensives (0.027 ± 0.003), but both groups attain similar high (˜ 0.074) rates when phosphorylation is stimulated by 0.5µmol/l phorbol 12-myristate 13-acetate (PMA) and similar low rates (˜0.01) when inhibited by 0.5nmol/l staurosporine. Furthermore, although hypertensive set-point is significantly (P+–H+ exchange in essential hypertension, rather than larger numbers of the exchanger per cell.

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