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Pinacidil opens K + ‐selective channels causing hyperpolarization and relaxation of noradrenaline contractions in rat mesenteric resistance vessels
Author(s) -
Videbæk Lars M.,
Aalkjær Christian,
Mulvany Michael J.
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb16553.x
Subject(s) - pinacidil , hyperpolarization (physics) , cromakalim , efflux , chemistry , membrane potential , biophysics , potassium channel opener , potassium channel , medicine , endocrinology , biology , biochemistry , stereochemistry , glibenclamide , agonist , receptor , nuclear magnetic resonance spectroscopy , diabetes mellitus
1 The effects of pinacidil on noradrenaline‐induced tone, smooth muscle membrane potential and 42 K‐ and 86 Rb‐efllux from isolated mesenteric resistance vessels (internal diameter 200 μm) of the rat have been studied. 2 Pinacidil (0.3–10 μ M ) produced concentration‐dependent suppression of noradrenaline‐induced tone. 3 Pinacidil (0.3–10 μ M ) caused concentration‐dependent hyperpolarization of the smooth muscle. 4 In rat resistance vessels loaded with 42 K, pinacidil (1–10 μ M ) significantly increased the 42 K‐efllux rate constant. 5 With the use of 86 Rb as a marker for K + , 1 μ M pinacidil did not affect the 86 Rb‐efflux rate constant, while 10 μ M pinacidil transiently increased the 86 Rb rate constant. 6 The results indicate that the relaxant action of pinacidil in these vessels is due to the opening of K + ‐channels and consequent hyperpolarization. The K + ‐channels opened are selective for 42 K over 86 Rb.