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AJP - Endocrinology and Metabolism, Vol 261, Issue 2 E240-E245, Copyright © 1991 by American Physiological Society
ARTICLES |
P. A. Naess, G. Christensen and F. Kiil
Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Norway.
To examine how atrial natriuretic factor (ANF) inhibits renin release during renal sympathetic nerve stimulation, experiments were performed in barbiturate-anesthetized dogs. In five dogs, intravenous ANF infusion (50 ng.min-1.kg body wt-1) reduced renin release induced by renal nerve stimulation (1 Hz) from 16.8 +/- 8.4 to 3.5 +/- 2.1 micrograms angiotensin I (ANG I)/min. In two groups, renin release was raised by ureteral occlusion, which enhances the effects of beta-adrenoceptor stimulation and increased prostaglandin synthesis. During ureteral occlusion, intrarenal infusion of isoproterenol (0.2 micrograms.min-1.kg body wt-1) increased renin release in eight dogs to 82.6 +/- 10.9 micrograms ANG I/min, which was not significantly reduced by ANF infusion (81.1 +/- 10.1 micrograms ANG I/min). Similarly, intrarenal infusion of arachidonic acid (80 micrograms.min-1.kg body wt-1) during ureteral occlusion increased renin release in five dogs to 22.2 +/- 3.0 micrograms ANG I/min, which was not significantly reduced by ANF infusion (22.5 +/- 3.5 micrograms ANG I/min). Finally, in six dogs examined at free urine flow, intrarenal infusion of phenylephrine, an alpha-adrenergic agonist, raised renin release from 0.5 +/- 0.3 to 20.1 +/- 6.8 micrograms ANG I/min, which was reduced to 10.6 +/- 3.9 micrograms ANG I/min by intravenous ANF infusion (100 ng.min-1.kg body wt-1). These results indicate that ANF does not counteract stimulation of renin release by beta-adrenoceptors and prostaglandins but reduces nerve-stimulated renin release by opposing alpha-adrenoceptor activity.
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