Blood Pressure Control

Abstract

Mechanisms responsible for the maintenance of high blood pressure have been investigated extensively in essential as well as in renovascular hypertension. The pathogenesis of hypertension in end-stage renal failure (ESRF), however, has evidently evoked little interest despite the fact that, due to a diminishing interference of the natural kidneys and an increasing potential allowing a modulation of several factors by the application of an artificial kidney, observations made in patients with advanced renal insufficiency would have been of great value for the elucidation of essential hypertension. Whereas the fractional sodium excretion is increased in mild or moderate renal insufficiency, this compensatory mechanism of the natural kidney is abolished in severe renal failure. Thus, hypertension in patients with renal insufficiency requiring artificial kidney treatment in most cases is a consequence of fluid and sodium overload. In a minor proportion of patients (about 10% of the dialysis population) hypertension may be volume independent, e.g., hypertension continues to exist in spite of adequate fluid removal. Whereas, an inverse relation exists between renin secretion and exchangeable sodium under physiological conditions [1], this individually determined equilibrium may be disturbed in those patients demonstrating an increased renin activity in spite of an augmentation of their exchangeable sodium (Fig.1). Disorders of the autonomic nervous system or catecholamine metabolism seem to be of minor importance, at least as factors for the maintenance of severe hypertension in advanced renal insufficiency.