title: Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats.
abstract: Abnormalities in the production and/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg/kg/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10(-9)-10(-4) M) and sodium nitroprusside (SNP, 10(-10)-10(-5) M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10(-3) M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.
authors: Department of Pharmacology, School of Medicine, Dicle University, Diyarbakir, Turkey. ogokalp@med.sdu.edu.tr
authors: O
authors: O
authors: Gökalp
authors: S
authors: S
authors: Ozdem
authors: S
authors: S
authors: Dönmez
authors: M
authors: M
authors: Dogan
authors: H
authors: H
authors: Demirin
authors: H Y
authors: HY
authors: Kara
authors: R
authors: R
authors: Sütcü
authors: E
authors: E
authors: Cicek
authors: M K
authors: MK
authors: Ozer
authors: N
authors: N
authors: Delibas
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D002104:Cadmium / Q000633:toxicity*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology
chemical_list: D002104:Cadmium; D009599:Nitroprusside; D009569:Nitric Oxide; D008315:Malondialdehyde; D001120:Arginine; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester