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Increased inward rectifier K + current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium‐dependent relaxation via Ca 2+ ‐activated K + channels
Author(s) -
Kim Hae Jin,
Yin Ming Zhe,
Cho Suhan,
Kim Sung Eun,
Choi Seong Woo,
Ye Sang Kyu,
Yoo Hae Young,
Kim Sung Joon
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13168
Subject(s) - hyperpolarization (physics) , medicine , inward rectifier potassium ion channel , chemistry , endocrinology , endothelium derived hyperpolarizing factor , patch clamp , vasodilation , endothelium , myocyte , depolarization , potassium channel , biophysics , electrophysiology , resting potential , biology , ion channel , receptor , stereochemistry , nuclear magnetic resonance spectroscopy
Abstract Endothelium‐dependent vasorelaxation is partly mediated by small‐conductance ( SK 3) and intermediate‐conductance Ca 2+ ‐activated K + channels ( SK 4) in the endothelium that results in endothelium‐dependent hyperpolarization ( EDH ). Apart from the electrical propagation through myoendothelial gap junctions, the K + released from the endothelium facilitates EDH by increasing inward rectifier K + channel (Kir) conductance in smooth muscle cells. The EDH ‐dependent relaxation of coronary artery ( CA ) and Kir current in smooth muscle cells ( CASMC s) of hypertensive animals are poorly understood despite the critical role of coronary flow in the hypertrophic heart. In spontaneously hypertensive ( SHR ) and control ( WKY ) rats, we found attenuation of the CA relaxation by activators of SK 3 and SK 4 ( NS 309 and 1‐ EBIO ) in SHR . In isolated CASMC s, whole‐cell patch‐clamp study revealed larger I Kir in SHR than WKY , whereas the myocytes of skeletal and cerebral arteries showed smaller I Kir in SHR than WKY . While the treatment with I Kir inhibitor (0.1 mmol/L Ba 2+ ) alone did not affect the WKY ‐ CA , the SHR ‐ CA showed significant contractile response, suggesting relaxing influence of the higher I K ir in the CASMC s of SHR . Furthermore, the attenuation of NS 309‐induced relaxation of CA by the combined treatment with 0.1 mmol/L Ba 2+ was more prominent in SHR than WKY . Our study firstly shows a distinct increase of I K ir in the CASMC s of SHR , which could partly compensate for the attenuated relaxation via endothelial SK 3 and SK 4.