The change of beta-adrenergic system in lead-induced hypertension

Citation
Da. Tsao et al., The change of beta-adrenergic system in lead-induced hypertension, TOX APPL PH, 164(2), 2000, pp. 127-133
Citations number
42
Categorie Soggetti
Pharmacology & Toxicology
Journal title
TOXICOLOGY AND APPLIED PHARMACOLOGY
ISSN journal
0041008X → ACNP
Volume
164
Issue
2
Year of publication
2000
Pages
127 - 133
Database
ISI
SICI code
0041-008X(20000415)164:2<127:TCOBSI>2.0.ZU;2-J
Abstract
Lead exposure is considered to be a risk factor of cardiovascular disease. To investigate the relationship between lead and cardiovascular disease/hyp ertension in lead exposure, beta-adrenergic system is explored in this stud y. We address three topics in this study: (a) the relationship between beta -adrenergic receptor and lead level in heart, aorta, and kidney of lead-exp osed rats; (b) the relationship between beta-adrenergic receptor in heart, aorta, kidney, and blood pressure in lead-exposed rats; and (c) the change of cyclic AMP level in heart, aorta, and kidney of rats with different lead levels. Wistar rats were chronically fed with 2, 1, 0.5, 0.1, 0.05, and 0. 01% lead acetate and water for 2 months. Plasma catecholamine level was mea sured by high-performance liquid chromatography. Radioligand binding assay was measured by a method that fulfilled strict criteria of beta-adrenocepto r using the ligand [I-125]iodocyanopindolol. Cyclic AMP (cAMP) level was de termined by radioimmunoassay. The levels of lead were determined by electro thermal atomic absorption spectrometry. The results showed that increased p lasma norepinephrine level, decreased aorta beta-adrenergic receptor and cA MP, and increased kidney beta-adrenergic receptor and cAMP contributed to t he elevation of blood pressure in lead-induced hypertension. The decrement of beta-adrenoceptor and cAMP in heart resulted in decreased contractility in heart. (C) 2000 Academic Press.