ENDOGENOUS NITRIC-OXIDE ON ARTERIAL HEMODYNAMICS - A COMPARISON BETWEEN NORMOTENSIVE AND HYPERTENSIVE RATS

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 hemodynami cs between spontaneously hypertensive rats (SHR) and normotensive Wist ar-Kyoto strain (WKY), 22-26 wk of age. In the first series of experim ents, various doses (1-30 mg/kg iv) of N-G-nitro-L-arginine methyl est er (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 incre ase in arterial pressure (AP) with a decrease in heart rate (HX). The maximal effects of L-NAhlE on AP and KR occurred at a dose of 10 mg/kg . Both the AP increase and HR decrease were higher in SHR (AP, +38 +/- 4 mmHg; KR, -49 +/- 5 beats/min) than WKY (AP, +22 +/- 3 mmHg; HR, -3 3 +/- 5 beat/min). In other series, the technique of impedance spectra l 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 i mpedance spectra. Both in WKY in = 12) and in SHR in = 12), L-NAME sig nificantly increased AP and total peripheral resistance (TPR). The pul satile and frequency-dependent hemodynamics including characteristic i mpedance, wave reflection, and ventricular work were only slightly alt ered. Despite higher resting values of AP and TPR in SHR (mean AP, 154 +/- 7 mmHg; mean TPR, 204 +/- 17 x 10(3) dyn.s.cm(-5)) than WKY (mean AP, 94 +/- 6 mmHg; mean TPR, 98 +/- 12 x 10(3) dyn.s.cm(-5)), the mag nitudes of AP and TPR increments after NO blockade were significantly higher in SHR (AP, +37 +/- 3 mmHg; TPR, +124 +/- 16 x 10(3) dyn.s.cm(- 5)) than in WKY (AP, +24 +/- 3 mmHg; TPR, +45 +/- 7 x 10(3) dyn.s.cm(- 5)). The continuous formation of endogenous NO affects predominantly t he AP and peripheral resistance in both WKY and SHR. The windkessel fu nctions, such as impedance spectra, pulse-wave reflection, and ventric ular work, are less affected after NO blockade. In addition, the effec ts of NO release on the AP and TPR appear to be enhanced in rats with established hypertension.