Renal effects of atrial natriuretic factor are independent of dopamine1 receptors.

This study examined whether the renal effects of atrial natriuretic factor (ANF) are mediated by dopamine1 (DA1) receptor activation. Intravenous infusion of low-dose ANF (0.0025 micrograms.kg-1.min-1) in euvolemic, pentobarbital sodium-anesthetized male mongrel dogs enhanced urine flow (V) by 71 +/- 14% (mean +/- SE) and urinary sodium excretion (UNaV) by 457 +/- 172% (P less than 0.05). Renal blood flow (RBF) was unchanged. Administration of pharmacological doses of ANF (0.1 microgram.kg-1.min-1) into the renal artery in volume-expanded dogs increased RBF by 26 +/- 6, V by 56 +/- 15, and UNaV by 101 +/- 42%. The selective DA1 receptor antagonist SCH-23390 (0.5 microgram.kg-1.min-1 iv) did not affect the response to ANF at either dose. The selective DA1 agonist, fenoldopam, increased RBF by 45 +/- 3, V by 94 +/- 27, and UNaV by 61 +/- 15% in volume-expanded dogs. With SCH-23390, fenoldopam increased RBF by only 16 +/- 6% whereas V and UNaV decreased by 16 +/- 10 and 17 +/- 10%, respectively. Accordingly, the failure of DA1 receptor-blocking doses of SCH-23390 to antagonize the response to ANF, at pharmacological or physiological doses, indicates that the renal effects of ANF, in the dog, are independent of DA1 receptor activation.