In vivo and in vitro effects of lead on vascular reactivity in rats.
Webb-RC; Winquist-RJ; Victery-W; Vander-AJ
Am J Physiol, Lung Cell Mol Physiol 1981 Aug; 241(2):H211-H216
Hypertension caused by increased vascular response to lead (7439921) was investigated in Wistar-rats. Rats were given drinking water containing 100 parts per million (ppm) lead as lead-acetate or sodium-acetate for 7 months. After sacrifice, tail arteries were excised and mounted in a holder connected to a force transducer. Strips of tail artery were electrically stimulated by two platinum wire electrodes parallel to the preparations. Arteries of untreated rats were equilibrated in physiologic salt solution containing either lead-acetate or sodium-acetate for 15 minutes before the addition of vasoactive agents or transmural nerve stimulation. Drugs used were norepinephrine-bitartrate (51401), methoxamine- hydrochloride (61165), and D-600 (16662478), a methoxy derivative of verapamil. Systolic blood pressures of rats treated with lead- acetate were significantly higher than those treated with sodium- acetate. Contractile responses to methoxamine or norepinephrine were significantly greater in tail artery strips treated with lead- acetate. Treatment of arterial strips with D-600 before addition of methoxamine similarly decreased the magnitude of contractile response in lead treated and sodium treated rats. Maximal contractile responses to electrical stimulation in tail artery strips from lead treated rats were significantly greater than in sodium treated rats. In-vitro experiments showed no effects on contractile responses to exogenous norepinephrine or electrical stimulation in sodium-acetate. The authors conclude that the experiments suggest a mechanism whereby chronic exposure to moderate lead concentrations could cause hypertension.
NIOSH-Publication; NIOSH-Grant; Cardiovascular-system; Lead-poisoning; Drinking-water; Chronic-exposure; In-vivo-study; Biological-effects; Cardiovascular-system-disease; Animal-studies; Blood-pressure;
Author Keywords: norepinephrine; D 600; methoxamine; vascular smooth muscle; tail artery
R. Clinton Webb, Physiology University of Michigan 6811 Medical Science II Ann Arbor, Mich
7439-92-1; 51-40-1; 61-16-5; 16662-47-8
Other Occupational Concerns; Grants-other
American Journal of Physiology: Lung Cellular and Molecular Physiology
University of Michigan at Ann Arbor, Ann Arbor, Michigan