Cardiovascular and renal effects of atrial natriuretic factor

Abstract

Atrial natriuretic factor (ANF) reduces cardiac output and systemic arterial blood pressure. The reduction in systemic arterial blood pressure is not caused by dilation of arterial resistance vessels, since total peripheral vascular resistance often increases during infusion of ANF. The reduction in cardiac output with subsequent hypotension can be explained by a decrease in venous return. The decrease in venous return is not due to pooling of blood in the capacitance vessels, since ANF reduces venous compliance. Reduced venous return during infusion of ANF can be explained by a reduction in circulating blood volume and an increase in resistance to venous return. The reduction in circulating blood volume is due to increased urine output and to a shift of circulating fluid into the interstitial space. The increase in renal sodium and water excretion is mediated by an increase in glomerular filtration rate and reduced sodium and chloride reabsorption in the collecting ducts. ANF also inhibits the renin-angiotensin-aldosterone system. The plasma level of ANF may be a parameter for the severity of heart diseases with increased preload. In congestive heart failure and supraventricular tachycardia, the increase in plasma ANF concentration may augment sodium excretion, but anti-natriuretic factors, such as reduction in renal perfusion pressure, may override the natriuretic effect of ANF. Reduced sodium excretion during mechanical ventilation with positive end-expiratory pressure (PEEP) is partly due to a decrease in ANF secretion.

Key Words:

• capacitance circulation
• cardiac output
• circulating blood volume
• congestive heart failure
• PEEP
• renal sodium excretion
• supraventricular tachycardia
• systemic blood pressure
• venous return