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Inhibition of human vascular smooth muscle cell proliferation by the novel multiple-action antihypertensive agent carvedilol

Patel, M.K., Chan, P., Betteridge, L.J., Schachter, M., Sever, P.S. (1995) Inhibition of human vascular smooth muscle cell proliferation by the novel multiple-action antihypertensive agent carvedilol. Journal of Cardiovascular Pharmacology, 25 (4). pp. 652-657. ISSN 0160-2446. (doi:10.1097/00005344-199504000-00020) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. (Contact us about this Publication)
Official URL
http://dx.doi.org/10.1097/00005344-199504000-00020

Abstract

We examined the antiproliferative effect of the novel multiple-action antihypertensive agent carvedilol on human vascular smooth muscle cells (VSMC). Carvedilol inhibited the increase in cell number induced by foetal calf serum (FCS) in 86% (18 of 21) of human VSMC grown both from saphenous vein (17.6 ± 3.5% inhibition, mean ± SEM, n = 15) and restenotic lesions (31.4 ± 5.5% inhibition, mean ± SEM, n = 5). Carvedilol had a greater antiproliferative effect than other (3-adrenoceptor antagonists. In comparison with calcium channel blockers, carvedilol (10 p.M) elicited a degree of growth inhibition similar to that of verapamil, but was less effective than the dihydropyridine amlodipine at equimolar concentrations. Although carvedilol had a greater antiproliferative effect on cells derived from restenotic lesions cells than on control saphenous vein cells, the difference was not statistically significant. In the present study, the antiproliferative effect of carvedilol on human VSMC in vitro occurred at concentrations higher than those in plasma. Although this may represent a limitation to the clinical efficacy of carvedilol against proliferation of VSMC associated with hypertension and atherosclerosis, the apparent relative selectivity of carvedilol for restenosis-derived cells is a promising line of investigation.

Item Type: Article
DOI/Identification number: 10.1097/00005344-199504000-00020
Uncontrolled keywords: Carvedilol, Cell proliferation, Human vascular smooth muscle, Myointimal hyperplasia, Restenosis, alpha 1 adrenergic receptor blocking agent, amlodipine, antihypertensive agent, beta adrenergic receptor blocking agent, calcium channel blocking agent, carvedilol, labetalol, propranolol, verapamil, antihypertensive activity, artery intima proliferation, article, cell proliferation, controlled study, dose response, drug effect, drug selectivity, growth inhibition, human, human cell, hypertension, priority journal, saphenous vein, vascular smooth muscle, Antihypertensive Agents, Calcium Channel Blockers, Carbazoles, Cell Division, Depression, Chemical, Human, Lactate Dehydrogenase, Muscle, Smooth, Vascular, Propanolamines, Saphenous Vein, Support, Non-U.S. Gov't, Thymidine, Vascular Diseases
Divisions: Faculties > Sciences > Kent and Medway Medical School
Depositing User: Philip Chan
Date Deposited: 07 Nov 2019 16:03 UTC
Last Modified: 07 Nov 2019 16:03 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/78344 (The current URI for this page, for reference purposes)
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