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Stretch-Activated Channels in Arterial Smooth Muscle of Genetic Hypertensive Rats
Author(s) -
Yusuke Ohya,
Natsuko Adachi,
Yoshito Nakamura,
Motoko Setoguchi,
Isao Abe,
Masatoshi Fujishima
Publication year - 1998
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.31.1.254
Subject(s) - depolarization , pipette , membrane potential , vascular smooth muscle , piezo1 , medicine , mesenteric arteries , stimulation , hyperpolarization (physics) , chemistry , biophysics , endocrinology , mechanosensitive channels , myocyte , ion channel , anatomy , artery , smooth muscle , biology , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
Electrical and contractile responses of small arteries to mechanical stress are reportedly enhanced in spontaneously hypertensive rats (SHR), compared with those in Wistar Kyoto rats (WKY). We have previously shown that stretch-activated cation channels exist in arterial smooth muscle membrane, of which opening causes Na+ and Ca2+ influx and membrane depolarization. We thus hypothesize that activation of stretch-activated channels is enhanced in arterial smooth muscle of SHR compared with WKY. To test this hypothesis, stretch-activated currents were recorded in single smooth muscle cells of resistance mesenteric arteries from SHR and WKY (16 to 24 weeks of age). In the whole-cell recording, membrane stretch was applied by inflating the cell with positive pressure to the recording pipette. Cell-inflation evoked Gd3+-sensitive cation currents. This current appeared with less stretch stimulation and its amplitude was larger in SHR cells compared with WKY cells. In the cell-attached recording, suction to the recording pipette evoked single stretch-activated channel currents (conductance of 32 pS with 150 mmol/L Na+), which were blocked by Gd3+. Channels were activated with less negative pressure and their availability was greater in SHR cells than in WKY cells. Results suggest that the activation of stretch-activated channels is enhanced in smooth muscle of resistance arteries from SHR compared with WKY, which may contribute to the enhanced vascular responses to mechanical stress in SHR.

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