Carvedilol inhibits basal and stimulated ACE production in human endothelial cells.

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Saijonmaa O, Nyman T, Fyhrquist F

Carvedilol inhibits basal and stimulated ACE production in human endothelial cells.

J Cardiovasc Pharmacol. 2004 May;43(5):616-21.

PubMed ID

15071347 [ View in PubMed

]

Abstract

Angiotensin-converting enzyme (ACE) plays an important role in the pathophysiology of cardiovascular disease. We examined the effect of carvedilol, a cardiovascular drug, on basal and stimulated ACE production in human endothelial cells. Carvedilol (0.625-5 microM), in a concentration-dependent manner, inhibited basal and vascular endothelial growth factor (VEGF, 0.5 nM) or phorbol 12-myristate 13-acetate (PMA, 10 nM) induced ACE up-regulation. Carvedilol has non-selective beta-adrenoceptor and selective alpha1-adrenoceptor blocking activity, calcium channel blocking, and anti-oxidant activity. To study whether these activities were related to ACE down-regulation, endothelial cells were treated with metoprolol (1-10 microM), propranolol (1-10 microM), prazosin (1-5 microM), nicardipine (1-10 microM), probucol (1-100 microM), or ascorbic acid (1-100 microM). None of these compounds modified ACE. VEGF (0.5 nM) and PMA (10 nM) induced PKC phosphorylation, which was inhibited by co-treatment of cell cultures with carvedilol (5 microM). In conclusion, carvedilol inhibited basal and VEGF or PMA induced ACE up-regulation. Inhibition of PKC phosphorylation was probably involved in carvedilol action.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Carvedilol	Vascular endothelial growth factor A	Protein	Humans	Unknown	Other	Details