On the physiological role of atrial natriuretic factor

Abstract

Atrial natriuretic factor, a family of peptides present in saline extract of cardiac atria, was discovered by deBold and colleagues in 1981. It was shown subsequently that ANF is synthesized in, and secreted from, myocytes in cardiac atria, that it circulates in the bloodstream, and that it acts on receptor sites in kidney and blood vessels. It is appropriate, therefore, to consider ANF as a new endocrine system which may be important in body fluid volume and blood pressure regulation. However, despite extensive investigation in many laboratories the regulatory roles of this hormone remain largely speculative. Although a causative contribution of endogenous ANF in the natriuretic response to acute hypervolemia is well established, its participation in the maintenance of salt balance during large variations in dietary Na intake is less certain. Depending on species studied (and laboratory) a range of more than 30-fold may or may not alter plasma levels of ANF, which, in any case, remain lower than those resulting in acute natriuresis. In addition to increased sodium excretion, atrial factor also inhibits aldosterone and renin release, both in vitro and in vivo. The in vitro effects occur at concentrations which are 10- to 100-fold higher than circulating plasma ANF levels. In addition, atrial factor reduces blood pressure when injected in the whole animal, and causes relaxation of precontracted smooth muscle in vitro. The vasorelaxant effect is detectable at concentrations which fall in the range of normal endogenous levels of the hormone. Although hypotension in vivo generally requires natriuretic doses of ANF, this may be due to compensatory reflexes in the intact animal.(ABSTRACT TRUNCATED AT 250 WORDS)