Intracellular Cation Concentrations in the Pathogenesis of Essential Hypertension

Abstract

As to the pathogenesis of essential hypertension numerous hypotheses have been proposed. In the last years a crucial role of cellular electrolyte metabolism has become more likely. First studies on cellular electrolyte metabolism in essential hypertension were performed by D’amico (1958) and Losse et al. (1960). These studies revealed an increase in intracellular Na⁺ concentration, which was later confirmed both in erythrocytes and in other blood cells (Edmondson et al. 1975; Ambrosioni et al. 1979; Fadeke-Aderounmu and Salako 1979; Forrester and Alleyne 1981; Hamlyn et al. 1982; Ringel et al. 1984). At the same time as the first studies on cellular electrolytes in essential hypertension, the existence of a natriuretic hormone was first suggested by De Wardener et al. (1961). They observed that saline infusion caused a natriuresis even with simultaneous administration of a mineralocorticoid, and concluded that this natriuresis could not be due to suppression of mineralocorticoid secretion. Later, the so-called natriuretic hormone was shown to inhibit cellular Na⁺-K⁺-ATPase (Gonick et al. 1977), thus increasing intracellular Na⁺ concentration and, possibly, causing natriuresis by inhibiting active tubular Na⁺ reabsorption. From these studies a relationship between an elevated intracellular Na⁺ concentration in essential hypertension and the secretion of a natriuretic hormone could be inferred. Therefore, it was hypothetized that hypertension due to volume expansion (Haddy and Overbeck 1976), and analogously, essential hypertension (De Wardener and MacGregor 1980) may be explained by the actions of the natriuretic hormone on cellular electrolyte metabolism.