Atrial natriuretic factor, the kidney and high blood pressure.

The discovery of atrial natriuretic factor (ANF) constitutes a major advance in our knowledge of negative cell regulatory pathways leading to vasodilation. The biochemical mechanisms of the action of ANF at the cellular level appear to be mediated by the cGMP- particulate guanylate cyclase system. In the kidney, the main cGMP increasing effect of ANF occurs at the level of the glomeruli, but it appears that action of ANF at the lowest part of the distal tubule is required for its natriuretic activity. Although most current knowledge concerning ANF has been obtained with pharmacological doses of the hormone, it appears that endogenous manipulations of ANF, such as those occurring with postural change, are associated with physiological consequences including increases of cGMP, natriuresis, and diuresis. In both experimental and human hypertension, increased plasma levels of ANF are secondary to higher blood pressure. In hypertension, the administration of ANF leads to an exaggerated renal response. We propose as a hypothesis that an abnormality in the expression of a vasodilatory system, such as ANF-cGMP, may play a role in the pathogenesis of hypertension.