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Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats

Department of Pharmacology, School of Medicine, Dicle University, Diyarbakir, Turkey, ogokalp{at}med.sdu.edu.tr

S. Özdem

Biochemistry Unit, Central Laboratory, School of Medicine, Akdeniz University, Antalya, Turkey

S. Dönmez

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

M. Dogan

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

H. Demirin

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

Y. Kara

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

R. Sütcü

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

E. Cicek

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

MK Özer

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

N. Delibas

Department of Biochemistry, School of Medicine, Süleyman Demirel University, Isparta, Turkey

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.

Key Words: acetylcholine • cadmium • hypertension • malondialdehyde • nitric oxide

This version was published on August 1, 2009

Toxicology and Industrial Health, Vol. 25, No. 7, 447-453 (2009)
DOI: 10.1177/0748233709106822


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