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Prostacyclin, endothelium-derived relaxing factor and vasodilatation.

G. Siegel, F. Schnalke, G. Stock, J. Grote

Open publisher page 14 citations

Abstract

In arterial smooth muscle with normal tone or predepolarized and precontracted by noradrenaline, prostacyclin (10(-9) to 10(-6) M) effects a dose-dependent hyperpolarization and relaxation. The hyperpolarization is due to K+ channel opening. In hypoxic vasodilatation, which is likewise induced by membrane hyperpolarization, a share of 20% falls to prostacyclin and 80% to an endothelium derived hyperpolarizing factor.

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What this paper is about

In arterial smooth muscle with normal tone or predepolarized and precontracted by noradrenaline, prostacyclin (10(-9) to 10(-6) M) effects a dose-dependent hyperpolarization and relaxation. The hyperpolarization is due to K+ channel opening. In hypoxic vasodilatation, which is likewise induced by membrane hyperpolarization, a share of 20% falls to prostacyclin and 80% to an endothelium derived hyperpolarizing factor.

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OpenAlex reports 14 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

In arterial smooth muscle with normal tone or predepolarized and precontracted by noradrenaline, prostacyclin (10(-9) to 10(-6) M) effects a dose-dependent hyperpolarization and relaxation. The hyperpolarization is due to K+ channel opening. In hypoxic vasodilatation, which is likewise induced by membrane hyperpolarization, a share of 20% falls to prostacyclin and 80% to an endothelium derived hyperpolarizing factor.

Key concepts: Hyperpolarization (physics), Prostacyclin, Vasodilation, Endothelium-derived hyperpolarizing factor, Endothelium, Internal medicine, Chemistry, Membrane potential

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