Endogenous nitric oxide (NO) plays an important role in maintaining a vasodilator tone. In the present study, we compared the effects of NO blockade on the steady and pulsatile components of arterial hemodynamics between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto strain (WKY), 22-26 wk of age. In the first series of experiments, various doses (1-30 mg/kg iv) of N^G-nitro-L-arginine methyl ester (L-NAME) were administered to block the NO release in anesthetized WKY and SHR. In both WKY and SHR, L-NAME caused a dose-dependent increase in arterial pressure (AP) with a decrease in heart rate (HR). The maximal effects of L-NAME on AP and HR occurred at a dose of 10 mg/kg. Both the AP increase and HR decrease were higher in SHR (AP, +38 ± 4 mmHg; HR, 49 ± 5 beats/min) than WKY (AP, +22 ± 3 mmHg; HR, 33 ± 5 beat/min). In other series, the technique of impedance spectral analysis was employed to investigate the effects of L-NAME (10 mg/kg iv) on the arterial hemodynamics. The aortic pressure and flow waves were recorded and subjected to Fourier transform for the analysis of impedance spectra. Both in WKY (n = 12) and in SHR (n = 12), L-NAME significantly increased AP and total peripheral resistance (TPR). The pulsatile and frequency-dependent hemodynamics including characteristic impedance, wave reflection, and ventricular work were only slightly altered. Despite higher resting values of AP and TPR in SHR (mean AP, 154 ± 7 mmHg; mean TPR, 204 ± 17 × 10³ dyn · s · cm⁵) than WKY (mean AP, 94 ± 6 mmHg; mean TPR, 98 ± 12 × 10³ dyn · s · cm⁵), the magnitudes of AP and TPR increments after NO blockade were significantly higher in SHR (AP, +37 ± 3 mmHg; TPR, +124 ± 16 × 10³ dyn · s · cm⁵) than in WKY (AP, +24 ± 3 mmHg; TPR, +45 ± 7 × 10³ dyn · s · cm⁵). The continuous formation of endogenous NO affects predominantly the AP and peripheral resistance in both WKY and SHR. The windkessel functions, such as impedance spectra, pulse-wave reflection, and ventricular work, are less affected after NO blockade. In addition, the effects of NO release on the AP and TPR appear to be enhanced in rats with established hypertension.