Evidence supporting a physiological role for proANP-(1-30) in the regulation of renal excretion

The experiments, performed in pentobarbital sodium-anesthetized rats, consi sted of a 1-h equilibration period followed by two 30-min control periods. Subsequently, synthetic rat pro atrial natriuretic peptide (ANP) [proANP-(1 -30)] (n = 8) was given as a bolus of 10 mug in 1 ml of 0.9% saline followe d by an infusion at 30 ng/min (20 mul/min) for six additional periods. Cont rol rats (n = 6) received only 0.45% saline in the appropriate volumes. Mea n arterial pressure, renal blood flow, and glomerular filtration rate did n ot change significantly in either group during the proANP-(1-30) infusion. Urine flow and potassium excretion increased similar to 50% in the proANP-( 1-30)-infused group only (P < 0.05). Sodium excretion and fractional excret ion of sodium, expressed as the change from their own baselines, were signi ficantly increased by the proANP-(1-30) infusion (P < 0.05), whereas cGMP e xcretion was similar in both groups. These results suggest that the rat seq uence of proANP-(1-30) produces a natriuresis in the rat independent of cha nges in hemodynamics and renal cGMP production. In a second study, rats (n = 8) were prepared as above and pretreated with 0.4 ml iv of rabbit serum c ontaining an antibody directed against proANP-(1-30) (anti-proANP group). T he rats were volume expanded with 3 ml of 6% albumin in Krebs and observed for 3 h to determine if the anti-proANP would attenuate the responses to vo lume expansion. Control rats (n = 7) received 0.4 ml of normal rabbit serum . The elevation in potassium excretion in response to volume expansion was significantly attenuated in the anti-proANP group (P < 0.05). Sodium excret ion and urine flow responses also tended to be reduced but not significantl y. These results suggest that in the rat, proANP-(1-30) plays a physiologic al role in regulating renal excretion.