title: The change of beta-adrenergic system after cessation of lead exposure.
abstract: For understanding a reversible or irreversible harm of beta-adrenergic system in lead induced cardiovascular disease (hypertension), We set up animal model to estimate the change of blood pressure and sympathetic nervous system after lead exposure withdrawn in the study. We address three topics in this study: (a) the relationship between withdrawal time of lead exposure and beta-adrenergic receptor, plasma catecholamine level, blood pressure, and lead level in heart, aorta, and kidney in lead-induced hypertensive rats after lead exposure stopped; (b) the relationship between blood pressure and beta-adrenergic receptor in heart, aorta, and kidney; (c) the estimation of relationship between lead withdrawn and the variation of beta-adrenergic system. Wistar rats were chronically fed with 2% lead acetate (experimental group) and water (control group) for 2 months. The rats were divided into 8 groups by withdrawal time of lead exposure stopped. Plasma catecholamine level was measured by high-performance liquid chromatography. Radioligand binding assay was measured by a method that fulfilled strict criteria of beta-adrenergic receptor using the ligand [125I]iodocyanopindolol. The levels of lead were determined by electrothermal atomic absorption spectrometry. The results showed that a close relation between reduced lead level and the plasma catecholamine level decreased, aorta beta-adrenergic receptor increased, kidney beta-adrenergic receptor diminished, heart beta-adrenergic receptor increased, and blood pressure dropped after lead exposure withdrawn. The study on the regulation of beta-adrenergic system in lead-induced hypertension after lead withdrawn might also provide insight about the nature of this disease state.
authors.affiliation: Department of Biomedical Engineering, I-Shou University, 1, Section 1, Shiuecheng Road, Dashu Shiang, Kaohsiung County, 840, Taiwan. huoy@isu.tw
authors.forename: Huoy-Rou
authors.initials: HR
authors.lastname: Chang
authors.forename: Der-An
authors.initials: DA
authors.lastname: Tsao
authors.forename: Hsin-Su
authors.initials: HS
authors.lastname: Yu
authors.forename: Chi-Kung
authors.initials: CK
authors.lastname: Ho
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D002395:Catecholamines / Q000097:blood; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009942:Organometallic Compounds / Q000493:pharmacokinetics / Q000633:toxicity*; D011485:Protein Binding; D011869:Radioligand Assay; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D014018:Tissue Distribution
chemical_list: D002395:Catecholamines; D009942:Organometallic Compounds; D011943:Receptors, Adrenergic, beta; C008261:lead acetate