The responsiveness of isolated high-pressure (aorta, renal artery) and low-pressure vessels (pulmonary artery) was compared during systemic hypertension induced by chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME) in rats. L-NAME (40 mg/kg/day) was given to animals in their drinking water. After 4 weeks of L-NAME treatment, systolic blood pressure increased by 37% as compared with that in the control group. Chronic L-NAME treatment resulted in significant reduction of endothelium-dependent relaxation to acetylcholine (10(-8) to 3 x 10(-6) mol/l) in both types of vessels. The reduced relaxation was not influenced by acute pretreatment with indomethacin (10(-5) mol/l), however, it was further reduced by acute pretreatment with additional L-NAME (10(-4) mol/l). L-arginine (10(-4) mol/l) improved the reduced relaxation. Endothelium-independent relaxation to sodium nitroprusside (10(-9) to 10(-6) mol/l) was unaffected by L-NAME treatment. beta-adrenoceptor-mediated relaxation to isoprenaline (10(-8) to 3 x 10(-6) mol/l) was also not influenced by chronic L-NAME treatment. Similar alterations in the responsiveness of high- and low-pressure vessels indicate rather the decisive role of nitric oxide restriction than that of elevated blood pressure in their development.

Institute of Normal and Pathological Physiology Slovak Academy of Sciences Bratislava Slovak Republic

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