The effects of nitric oxide (NO) inhibition on sympathetic outflow is dependent on angiotensin II (All)

Increasing evidence suggests that endogenous NO inhibits sympathetic outflow in anesthetized animals. However, in a previous study (Circulation 92:1-13,1995) we were unable to find any evidence of increased renal sympathetic nerve activity (RSNA) in response to blockade of NO synthesis in conscious rabbits. One factor for this discrepancy may be the difference in the resting level of systemic AH, which may be lower in well trained, conscious animals. In the present study the effects of blockade of NO synthesis with nitro-L-arginine methyl ester (L-NAME) on the resting RSNA with and without a background infusion of All was investigated in conscious rabbits. In order to minimize baroreflex influences on RSNA, arterial pressure was returned to control levels by infusion of hydralazine. The data are shown in the table below. RSNA was increased above control only after L-NAME was given following All infusion. These data suggest that All enhances the effect of blockade of NO synthesis on sympathetic outflow in conscious rabbits. MAPÇmmHg) RSNA(%) MAP(mmHg) RSNA(%) Control 83.6±3.9 100.0±0 All 94.8±1.8 100.0±0 L-NAME 92.7±4.2' 29.7±6.0" L-NAME 112.0±5.8 57.5±6.4 Hydra 81.4±3.9 76.06.4 Hydra 95.2±1,8 178.0±18.1 p<.05 compared to control or All, Hydra=hydralazine.