Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats
TOXICOLOGY AND INDUSTRIAL HEALTH, cilt.25, sa.7, ss.447-453, 2009 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 25 Sayı: 7
- Basım Tarihi: 2009
- Doi Numarası: 10.1177/0748233709106822
- Dergi Adı: TOXICOLOGY AND INDUSTRIAL HEALTH
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.447-453
- Anahtar Kelimeler: acetylcholine, cadmium, hypertension, malondialdehyde, nitric oxide, NITRIC-OXIDE SYNTHASE, LIPID-PEROXIDATION, BLOOD-PRESSURE, AORTIC RINGS, RESPONSIVENESS, INHIBITION, TOXICITY, EXPRESSION, EXPOSURE, CHLORIDE
- Akdeniz Üniversitesi Adresli: Evet
Özet
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.