Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inh ibitor, N-G-nitro-L-arginine methyl ester (L-NAME), in conscious rats. In t he 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but si gnificantly increased HR and RSNA by 88 +/- 12 beats/min and 67 +/- 12%, re spectively. Intravenous infusion of L-NAME (50 mu g.kg(-1).min(-1)) signifi cantly attenuated these tachycardic and sympathoexcitatory responses to hem orrhage (14 +/- 7 beats/min and 26 +/- 12%, respectively). Pretreatment of L-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses in duced by L-NAME (92 +/- 6 beats/min and 64 +/- 10%, respectively). L-NAME b y itself did not alter the baroreceptor reflex control of HR and RSNA. Hemo rrhage increased the plasma vasopressin concentration, and its increment in the L-NAME-treated group was significantly higher than that in the 0.9% sa line group. Pretreatment with the vascular arginine vasopressin V-1-recepto r antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced by L-NAME (54 +/- 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the barorecep tor reflex arch. It can be assumed that NO modulated the baroreflex functio n by altering the secretion of vasopressin induced by hemorrhage.