Key result
Pinacidil and TEA affected contractions to 5-HT and noradrenaline, but contractions to endothelin-1 were only minimally affected, suggesting its mechanism does not involve membrane depolarization.
Why the study?
The mechanisms by which endothelin-1 contracts rat pulmonary artery and the role of potassium channels in this process were unclear.
Endothelin-1 induced contractions in rat pulmonary artery do not involve membrane depolarization or calcium entry through voltage-operated calcium channels, unlike contractions induced by noradrenaline or 5-HT.
ET-1 contractions appear depolarization-independent in vitro; leaves open relevance to clinical vascular tone or targeted therapies.
The effects of the potassium channel opening drug, pinacidil, and the potassium channel closing drug, tetraethylammonium (TEA), on concentration-response (contraction) curves to spasmogens on rat pulmonary artery were examined. Pinacidil (3 microM) decreased, and TEA (2 mM) increased contractions to 5-hydroxytryptamine (5-HT) more than it did to noradrenaline but contractions to endothelin-1 were only minimally affected. It is concluded that the mechanism whereby endothelin-1 contracts rat pulmonary artery differs from that of noradrenaline or 5-HT in that it does not involve membrane depolarization or calcium entry through voltage operated calcium channels.
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Wanstall et al. (1991) studied this question. Pinacidil and tetraethylammonium (TEA) was evaluated on Contractions to spasmogens (5-HT, noradrenaline, endothelin-1). Pinacidil and TEA affected contractions to 5-HT and noradrenaline, but contractions to endothelin-1 were only minimally affected, suggesting its mechanism does not involve membrane depolarization.
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