Circulating Natriuretic Factor in the Pathogenesis of Genetic Hypertension of Renal Origin

Abstract

A circulating natriuretic factor, able to inhibit the cellular Na⁺-K⁺ pump, has been described in human essential and animal sperimental hypertension (1,2). Increases of this circulating factor seem to be linked to a kidney defect in sodium and water excretion. The Milan hypertensive strain of rats (MHS) spontaneously develops hypertension due to a genetically determined, renal abnormality which produces a transient Na retention during the prehypertensive phase (3). To verify whether a circulating natriuretic factor could be involved in the pathogenesis of MHS hypertension, we have measured in MHS and their normotensive controls (MNS) at different ages the Na transport through the Na⁺-K⁺ pump in red blood cells (RBC), and the ability of rat plasma to stimulate “in vitro” the glucose 6-phosphate-dehydrogenase (G6PD) as index of the plasma capacity to inhibit the Na⁺-K⁺ ATPase activity(4).