title: Restriction of nitric oxide rather than elevated blood pressure is responsible for alterations of vascular responses in nitric oxide-deficient hypertension.
abstract: 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.
authors.affiliation: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
authors.forename: A
authors.initials: A
authors.lastname: Holécyová
authors.forename: J
authors.initials: J
authors.lastname: Török
authors.forename: I
authors.initials: I
authors.lastname: Bernátová
authors.forename: O
authors.initials: O
authors.lastname: Pechánová
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D011652:Pulmonary Circulation / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D007545:Isoproterenol; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine; D007213:Indomethacin