We have previously demonstrated that atrial natriuretic peptide (ANP) completely reverses norepinephrine-induced afferent arteriolar (AA) vasoconstriction. In the present study we characterized the effects of ANP on pressure-induced vasoconstriction of AA. Chronic unilateral hydronephrosis was induced to facilitate direct visualization of the renal microcirculation. Hydronephrotic kidneys were perfused in vitro, and AA diameters were measured during stepwise alterations in renal arterial pressure. Increasing renal arterial pressure from 80 to 180 mm Hg decreased AA diameter by 22 ± 2% (from 18.5 ± 1.0 to 14.4 ± 1.0 μm, p < 0.005). In the presence of 100 nM ANP [human ANP-(4-28)], AA vasoconstricted by 23 ± 4%, indicating that ANP failed to modify the pressure-induced AA vasoconstriction. Furthermore, both nitroprusside (10 μM) and 8-bromoguanosine 3':5'-cyclic monophosphate (30 μM) only partially inhibited pressure-induced AA vasoconstriction (31 ± 5% and 47 ± 7%, respectively), whereas these vasodilators completely abolished norepinephrine-induced AA vasoconstriction. In contrast, nifedipine completely inhibited pressure-induced AA vasoconstriction. In summary, pressure-induced AA vasoconstriction is insensitive to the action of ANP, is relatively refractory to cyclic GMP-mediated vasorelaxation, but is completely inhibited by calcium channel blockade. Furthermore, since ANP completely abolishes norepinephrine-induced vasoconstriction but fails to affect pressure-induced vasoconstriction, it is apparent that the type of underlying vasoconstrictor stimuli constitutes a major determinant of the renal microvascular response to ANP.
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