Nattaporn YoopanPiyajit WatcharasitOrapin WongsawatkulPawinee PiyachaturawatJutamaad SatayavivadMahidol UniversitySrinakharinwirot UniversityChulabhorn Research Institute2018-07-122018-07-122008-01-30Toxicology Letters. Vol.176, No.2 (2008), 157-161037842742-s2.0-37549064778https://repository.li.mahidol.ac.th/handle/20.500.14594/19881Cadmium (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. © 2007 Elsevier Ireland Ltd. All rights reserved.Mahidol UniversityPharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1016/j.toxlet.2007.11.002