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Endothelium‐dependent relaxation and hyperpolarization of canine coronary artery smooth muscles in relation to the electrogenic Na‐K pump
Author(s) -
Chen Guifa,
Hashitani Hikaru,
Suzuki Hikaru
Publication year - 1989
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.1476-5381.1989.tb14625.x
Subject(s) - hyperpolarization (physics) , ouabain , membrane potential , acetylcholine , atropine , biophysics , chemistry , endothelium , medicine , endocrinology , biology , stereochemistry , sodium , organic chemistry , nuclear magnetic resonance spectroscopy
1 In the smooth muscle cells of canine coronary artery, acetylcholine (ACh) produced a transient, endothelium‐dependent hyperpolarization of the membrane. A similar hyperpolarization was also elicited by exposure to Krebs solution after incubation of the artery in K‐free solution for 30 min. 2 A hyperpolarization of reproducible amplitude was generated when ACh was applied at intervals greater than 30 min. Repetitive application of ACh at 15 min intervals caused a successive reduction in the amplitude of hyperpolarization. 3 The reduction in the amplitude of relaxation during five successive applications of ACh at 15 min intervals was less than 10% of the first relaxation. 4 The ACh‐induced hyperpolarization was blocked by atropine but not by ouabain, whereas the K‐free induced hyperpolarization was blocked by ouabain. In low Na (Li‐substituted) solution, ACh still induced a hyperpolarization but the K‐free induced hyperpolarization was absent. 5 In coronary artery precontracted by high‐K solution, ACh produced an endothelium‐dependent relaxation, without membrane hyperpolarization. The associated relaxation was resistant to ouabain but sensitive to atropine. 6 It is concluded that in the canine coronary artery, the electrogenic Na‐K pump does not contribute to the endothelium‐dependent hyperpolarization or relaxation. The results are consistent with the release of two different inhibitory factors from the vascular endothelium.