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Hypoxia‐induced inhibition of calcium channels in guinea‐pig taenia caeci smooth muscle cells
Author(s) -
Rekalov Vladimir,
Juránek Ivo,
Máleková L'ubica,
Bauer Viktor
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.107bc.x
Subject(s) - biophysics , chemistry , hypoxia (environmental) , contraction (grammar) , hyperpolarization (physics) , guanethidine , pipette , calcium , endocrinology , potassium channel , medicine , biology , stereochemistry , stimulation , oxygen , organic chemistry , nuclear magnetic resonance spectroscopy
1 The effects of hypoxia on whole‐cell current in single smooth muscle cells and on a high K + ‐induced contraction of strips of the guinea‐pig taenia caeci were studied. 2 In physiological salt solution (PSS) and K + ‐based pipette solution, hypoxia ( P O 2 = 20 mmHg) reversibly inhibited both the inward Ca 2+ current ( I Ca ) and outward Ca 2+ ‐activated K + current ( I K(Ca) ) components of the whole‐cell current. 3 In PSS and Cs + ‐based pipette solution, hypoxia reversibly suppressed I Ca by 30 ± 5% at 0mV. 4 When Ba 2+ was used as a charge carrier, the I Ba was suppressed by hypoxia in a potential‐dependent manner, with the maximum of 40 ± 7% at +10mV. Alterations of concentrations of egta , GDBβS or ATP in the pipette solution did not change the inhibitory effects of hypoxia on I Ca and I Ba . 5 In PSS with 2 mm CaCl 2 replaced by CoCl 2 , hypoxia did not affect the Ca 2+ influx‐independent potassium current. 6 In cells voltage clamped at ‐20 mV hypoxia reversibly inhibited the spontaneous transient outward currents. 7 The response of high K + ‐contracted taenia caeci to hypoxia was composed of an initial rapid relaxation followed by a small transient contraction and slow relaxation. The transient contraction was blocked by atropine (1–10 μ m ), while relaxations were unaffected by atropine and guanethidine (10 μ m ). 8 The results show that hypoxia reversibly inhibits I Ca and secondarily suppresses I K(Ca) due to decreased Ca 2+ influx through Ca 2+ channels. 9 It is suggested that inhibition of I Ca was responsible for the rapid relaxation, whereas transient contraction may have been due to release of acetylcholine from nerve terminals upon hypoxia.