Direct vasodilatory action of atrial natriuretic factor on canine glomerular afferent arterioles

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Abstract
Studies were performed to examine whether atrial natriuretic peptide (ANP) has a direct action on glomerular afferent arterioles, and if so, whether the action is mediated by guanosine 5''-cyclic monophosphate (cGMP). A single superficial afferent arteriole was dissected from the canine kidney and perfused with the single glomerular perfusion technique described by Osgood et al. [Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13):F349-F354, 1983]. Norepinephrine (NE, 1 .times. 10-6 M) significantly increased arteriolar resistance, calculated from the perfusion rate and arteriolar pressure. Synthetic human ANP (hANP) provoked afferent arteriolar dilation and attenuated the NE-induced increase in arteriolar resistance with 1 .times. 10-10 to 1 .times. 10-6 M concentrations. This vasodilatory effect was significantly potentiated by 2-o-propoxyphenyl-8-azapurin-6-one (M and B 22,948, 4 .times. 10-12 M), a cGMP phosphodiesterase inhibitor, probably due to a sequential interaction of synergistic drugs. Also, the 1 .times. 10-4 M concentration of 8-bromoguanosine 5''-cyclic monophosphate or dibutyryl guanosine, 5''-cyclic monophosphate (DBcGMP) lessened NE-induced arteriolar constriction, but DBcAMP did not. We conclude from these observations that ANP has a direct vasodilatory action on canine glomerular afferent arterioles, and that this ANP-induced vasodilation is mediated by enhanced cGMP synthesis.