The effect of SNP-induced hypotension on the sympatho-adrenal nerve activity (SANA) was studied in enflurane anesthetized rats. Anesthesia was maintained with enflurane (2.2%) in 50% O2, and the rats were ventilated to achieve an end-tidal CO2 of 40 +/- 5 mmHg after giving pancuronium bromide. A bundle of the left adrenal nerves was dissected under a microscope and placed on a pair of platinum wire electrodes during SNP-induced hypotension for measurement of SANA. SNP was administered at 33-66 micrograms.kg-1.hr-1 for 20 minutes to maintain the mean arterial pressure (MAP) of 60% of the MAP before SNP infusion. SANA was measured for 45 minutes from 5 minutes before SNP infusion to 20 minutes after cessation of SNP infusion. When MAP was lowered, SANA increased by 80.2% (P less than 0.05), 29.4% (P less than 0.05) and 0%, in control group (n = 6), baroreceptor denervated group (n = 5) and baroreceptor denervated and bilateral renal vessel ligated group (n = 5), respectively. In order to study the mechanism in which the kidney may be involved, SANA during SNP-induced hypotension was measured before and after intravenous infusion of angiotensin II competitive inhibitor, [Sar1, Ile8] angiotensin II (SI-AII), (n = 5). Before SI-AII infusion, SANA increased by 31.2% during SNP-induced hypotension, but after SI-A II infusion, SANA during SNP-induced hypotension increased by 13.6%. (P less than 0.05; vs. before SI-AII infusion). There was no evidence of acidosis due to cyanide toxicity, hypoglycemia and profound hypotension, which make SANA increase. Therefore I concluded that SANA increased by 80.2% during SNP-induced hypotension, and that the increase in SANA was mediated by baroreceptor and kidney. And among the mechanism which the kidney is involved in, angiotensin II was suggested to be responsible for SANA increase during SNP-induced hypotension.