Inhibition of lymphocyte sodium pumps by a low serum concentration of potassium in essential hypertension

Abstract

Abnormal sodium pump transport of cations in human leukocytes increased the intracellular concentration of Na+ in essential hypertension. External K+ concentration in part determines sodium pump function in leukocytes; a reduced serum K+ concentration ([K+]) may inhibit sodium pump transport in vivo. We decided to measure serum K+ concentration and ouabain sensitive 86Rb+ influx (RI), an estimate of K+ influx rate, in lymphocytes from patients with mild essential hypertension. Mean serum [K+] was significantly lower in lymphocytes from 32 hypertensive patients (4.07 ± 0.30) than 53 healthy subjects (4.39 ± 0.36 mmol l-1), but mean RI was similar in the two groups. We also compared serum [K+] and RI in cells from 9 hypertensive patients before and after treatment with β-adrenoceptor antagonists. Mean serum [K+] after effective treatment was similar to that before treatment. However, mean RI was significantly higher after than before treatment. We also measured the effect of external [K+] on K+ influx rate in normal lymphocytes in vitro. Mean K+ influx rate was progressively reduced by decreasing external concentrations of K+. The reduction in serum [K+] in young patients with mild hypertension might contribute to inhibition of sodium pump function in vivo in hypertension. β-Adrenoceptor blockade increases the activity of sodium pumps per cell in essential hypertension. This effect may be due to a direct action of β-adrenoceptor antagonists on the sodium pump.