Biotin improves relaxation of rat aortic rings in combination with antihypertensive drugs

Abstract

Biotin at pharmacological concentrations has beneficial effects on hypertriglyceridaemia, hyperglycaemia and hypertension. We recently reported in a model of metabolic syndrome that biotin has an antihypertensive effect and decreases arterial contraction. In this study, we investigated the effect of biotin (10 nM) on arterial contraction in rat aortic rings with or without an endothelium induced by phenylephrine (1 × 10−9 to 1 × 10−5 M) or calcium (1 × 10−6 to 1 × 10−2.5 M) in the presence of antihypertensive drugs (BMY 7378, 100 nM; captopril, 1 μM; or nitrendipine, 100 nM). Biotin suppressed phenylephrine-induced vasoconstriction, which is partly modulated via endothelium-independent mechanisms. Biotin incubation with BMY 7378, captopril or nitrendipine improved the vasorelaxant effects of these drugs on aortic rings contracted by phenylephrine or calcium. Moreover, biotin decreased arterial contraction induced by calcium, suggesting the inhibition of extracellular influx and intracellular release of calcium. Our data demonstrate for the first time that biotin enhanced the vasorelaxant effect of some antihypertensive drug classes in rat aortic rings. Therefore, biotin could be used as a therapeutic strategy together with antihypertensive drugs for the treatment of hypertension.