Atrial natriuretic factor modulates proximal glomerulotubular balance in anesthetized rats.

The extent to which the natriuretic effect of a prolonged low dose infusion of atrial natriuretic factor (30 ng/kg/min) is dependent on interference with the prevailing intrarenal actions of angiotensin II was examined before and after blockade of angiotensin production with the converting enzyme inhibitor enalaprilat (5 mg/kg). Lithium clearance was used to assess proximal tubular sodium and water reabsorption. Atrial natriuretic factor and enalaprilat caused similar increases in sodium excretion (10-fold and sevenfold, respectively) and glomerular filtration rate (each 34%) and similar decreases in fractional proximal reabsorption of sodium (17% and 13%, respectively) and blood pressure. Each also caused a major disruption in the effectiveness of proximal glomerulotubular balance (30% and 50% of perfect balance). Infusion of atrial natriuretic factor during converting enzyme inhibition increased glomerular filtration rate further by 23%, reaching 63% above control without change in renal blood flow but with a rise in filtration fraction to 0.48. Sodium excretion increased further but fractional proximal sodium reabsorption remained constant and proximal glomerulotubular balance appeared to improve. Atrial natriuretic factor therefore possesses a glomerular action that persists during converting enzyme inhibition and is indeed additive to the removal of angiotensin II when the proximal effect of atrial natriuretic factor is no longer apparent. It is concluded that failure of atrial natriuretic factor to further suppress fractional proximal sodium reabsorption during converting enzyme inhibition is caused by either prior removal of the stimulatory action of angiotensin II on proximal tubular transport or extreme changes in peritubular physical factors consequent on the high filtration fraction.