The hemodynamic actions of N-nitro-L-arginine (L-NNA), a novel NO synthesis inhibitor, and its effect on renal sympathetic nerve activity (RSNA) were examined in anesthetized rats to define the possible role of L-NNA in the regulation of blood pressure and the underlying mechanism(s). The results obtained were as follows. (1) Following intravenous bolus injection of L-NNA (15 mg/kg), MAP was changed from 9.87 +/- 0.80 to 14.67 +/- 0.53 kPa (P < 0.001), HR from 317 +/- 13 to 303 +/- 14 bpm, CI from 9.79 +/- 0.83 to 7.04 +/- 0.41 ml/min.100 g-1 (P < 0.05), and TPRI from 1.04 +/- 0.10 to 2.15 +/- 0.18 u/100 g (P < 0.001), all lasting for more than 30 min. The above-mentioned actions of L-NNA could be inhibited by prior administration of L-arginine (200 mg/kg). (2) In rats with sinoaortic denervation (SAD), i.v. L-NNA might induce an increase in HR, indicating that L-NNA-induced bradycardia was resulted from a baroreceptive activation. (3) In rats with buffer nerves intact, i.v. L-NNA failed to induce a significant change in RSNA, though an increase in MAP accompanied by bradycardia was observed. (4) With i.v. L-NNA for SAD rats, MAP, HR and RSNA were markedly increased by 55.6%, 5.1% and 34.3%, respectively. The results implied that L-NNA was able to activate sympathetic center, and L-NNA-induced change of RSNA could be masked by baroreflex. Prior administration of L-arg was capable of inhibiting the effect of L-NNA on RSNA in SAD rats.(ABSTRACT TRUNCATED AT 250 WORDS)