1 We employed the technique of impedance spectral analysis to investigate the role of endogenous nitric oxide (NO) in the regulation of steady and pulsatile haemodynamics in Wistar Kyoto rat (WKY). 2 A total of 12 WKYs was anaesthetized with pentobarbitol sodium (40 mg kg 71 , i.p.) and arti®cially ventilated with an animal respirator. The aortic pressure wave was monitored with a high ®delity Millar sensor, and aortic¯ow wave with an electromagnetic¯ow probe. The pressure and¯ow waves were subjected to Fourier transform for the analysis of impedance spectra. 3 The baseline cardiovascular parameters were mean arterial pressure (APm) 95+9 mmHg, heart rate (HR) 338+9 b.p.m., stroke volume (SV) 0.23+0.01 ml, cardiac output (CO) 77.8+1.6 ml min 71 , total peripheral resistance (TPR) 98+11 (610 3 ) dyne s cm 75 , characteristic impedance (Zc) 2046+141 dyne s cm 75 , arterial compliance at mean AP (Cm) 3.78+0.22 ml mmHg 71 and backward pulse wave (P b ) 12.9+0.6 mmHg. 4 An NO synthase inhibitor, N G -nitro-L-arginine monomethyl ester (L-NAME) was administered at graded intravenous doses. This agent caused dose-dependent increases in AP and TPR with decreases in HR. At an accumulative dose of 10 mg kg 71 , APm was increased by 29+3 mmHg (+31%) and TPR by 49+6 (610 3 ) dyne s cm 75 (+50%), while HR was reduced by 37+5 b.p.m. (711%) and CO by 10.4+0.8 ml min 71 (714%). The pulsatile haemodynamics including Zc and P b were slightly increased by 14 ± 15%. Cm was decreased by 1.09 ml mmHg 71 (729%). L-NAME also did not signi®cantly a ect the ventricular work including the steady, oscillatory and total work. 5 Aminoguanidine, a speci®c inhibitor for inducible NO synthase (iNOS), in dose 10 ± 60 mg kg 71 i.v. did not alter the AP, HR and other parameters. The result indicated that blockade of constitutive NOS, but not iNOS is involved in these changes. 6 Angiotensin II (Ang) in various infusion doses was used to produce a pro®le of AP increase similar to that caused by L-NAME. Ang remarkably increased Zc, while TPR was moderately elevated. The pattern of haemodynamic changes was di erent from that following L-NAME. 7 The results suggest that blockade of the endogenous NO a ects predominantly the arterial pressure and peripheral resistance. The Windkessel functions such as arterial impedance and pulse wave re¯ection are slightly increased. Ventricular works are not signi®cantly altered.