BASAL NITRIC-OXIDE PRODUCTION CURTAILS ARTERIOLAR VASOCONSTRICTOR RESPONSES TO ANG-II IN RAT-KIDNEY

Experiments were performed to test the hypothesis that renal arteriola r vasoconstrictor responses to angiotensin II (ANG II) are curtailed t hrough a mechanism that involves stimulation of endogenous nitric oxid e (NO) synthesis. The in vitro blood-perfused juxtamedullary nephron t echnique was exploited to monitor arteriolar lumen diameter responses to exogenous ANG II before and during treatment with the NO synthase i nhibitor N(omega-)nitro-L-arginine (L-NNA). Under control conditions, 1 nM ANG II reduced afferent and efferent arteriolar diameters by 13 a nd 11%, respectively. In the presence of L-NNA, 1 nM ANG II decreased afferent diameter by 26% and efferent diameter by 35%. This augmentati on could not be attributed to the L-NNA-induced decrease in baseline d iameter. L-NNA also augmented vasopressin responses, indicating a lack of agonist specificity in this interaction. ANG II reactivity during L-NNA treatment was not enhanced when tissue NO activity was fixed at basal levels (exposure to 1 mu M sodium nitroprusside). These results indicate that endogenous NO modulates the vasoconstrictive impact of A NG II on both afferent and efferent arterioles of juxtamedullary nephr ons and that this process does not require stimulation of NO synthesis .