Basal nitric oxide production curtails arteriolar vasoconstrictor responses to angiotensin II in rat kidney.

The purpose of the present study was to probe the hypothesis that endogenous NO counteracts angiotensin II (AngII)-induced renal arteriolar vasoconstriction through a mechanism involving stimulation of NO synthesis. Using the in vitro blood-perfused juxtamedullary nephron technique, afferent (AFF) and efferent (EFF) arteriolar lumen diameter responses to AngII were measured before (untreated) and during exposure to a NO synthesis inhibitor (100 μM nitro-L-arginine, NLA). NLA significantly reduced baseline diameters of both AFF (21.5±1.8 to 17.2±1.3 μm) and EFF (21.3±2.2 to 17.5± 2.1 μm), and enhanced AngII responsiveness. In some NLA-treated kidneys, basal tissue NO levels were restored by exposure to an exogenous NO donor (sodium nitroprusside, SNP) at a concentration (1μM) which returned arteriolar diameters to baseline values. Despite continued inhibition of endogenous NO synthesis, AngII responses after restoration of basal NO levels (NLA + SNP) were identical to those observed under untreated conditions. Additional experiments verified that these responses could not be attributed to differences in baseline diameter per se. On the basis of these observations, we conclude that basal endogenous NO synthesis is sufficient to counteract arteriolar vasoconstriction induced by exogenous AngII in rat kidney.