title: Attenuation of eNOS expression in cadmium-induced hypertensive rats.
abstract: Cadmium (Cd) has been reported to induce hypertension in both humans and animals; however, its mechanism has not been clearly elucidated. Vascular tone is one of the factors contributing to hypertension. This study was conducted to investigate the effects of Cd exposure on vascular muscarinic receptor responses to acetylcholine (ACh) in isolated aortas. Male Sprague-Dawley rats were exposed to Cd via drinking water (5, 10 and 50 ppm) for 3 months. Cd 10 and 50 ppm exposure caused significant decreases in the sensitivity of vascular muscarinic receptors to ACh. However, Cd exposure did not alter the vascular relaxation induced by sodium nitroprusside (SNP) which is a nitric oxide donor. Consistent with the reduction of ACh-induced relaxation, treatment with Cd decreased endothelial nitric oxide synthase (eNOS) protein level in blood vessels. These results suggested that Cd suppressed ACh-induced vascular relaxation by interfering with muscarinic receptor function, and its downstream signaling pathway may be one of the contributing factors for the development of hypertension.
authors.affiliation: Toxicology Graduate Programme, Faculty of Science, Mahidol University, Rama 6 Rd., Bangkok 10400, Thailand.
authors.forename: Nattaporn
authors.initials: N
authors.lastname: Yoopan
authors.forename: Piyajit
authors.initials: P
authors.lastname: Watcharasit
authors.forename: Orapin
authors.initials: O
authors.lastname: Wongsawatkul
authors.forename: Pawinee
authors.initials: P
authors.lastname: Piyachaturawat
authors.forename: Jutamaad
authors.initials: J
authors.lastname: Satayavivad
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D015153:Blotting, Western; D019256:Cadmium Chloride / Q000008:administration & dosage / Q000737:chemistry / Q000633:toxicity*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D004785:Environmental Pollutants / Q000008:administration & dosage / Q000737:chemistry / Q000633:toxicity; D006973:Hypertension / Q000139:chemically induced / Q000201:enzymology* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043587:Receptor, Muscarinic M3 / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects; D014666:Vasomotor System / Q000187:drug effects / Q000378:metabolism
chemical_list: D004785:Environmental Pollutants; D020030:Nitric Oxide Donors; D043587:Receptor, Muscarinic M3; D009599:Nitroprusside; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D019256:Cadmium Chloride; D000109:Acetylcholine