Hypoxia‐induced inhibition of calcium channels in guinea‐pig taenia caeci smooth muscle cells

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<jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>The effects of hypoxia on whole‐cell current in single smooth muscle cells and on a high K<jats:sup>+</jats:sup>‐induced contraction of strips of the guinea‐pig taenia caeci were studied.</jats:p></jats:list-item> <jats:list-item><jats:p>In physiological salt solution (PSS) and K<jats:sup>+</jats:sup>‐based pipette solution, hypoxia (<jats:italic>P</jats:italic>O<jats:sub>2</jats:sub>= 20 mmHg) reversibly inhibited both the inward Ca<jats:sup>2+</jats:sup> current (<jats:italic>I</jats:italic><jats:sub>Ca</jats:sub>) and outward Ca<jats:sup>2+</jats:sup>‐activated K<jats:sup>+</jats:sup> current (<jats:italic>I</jats:italic><jats:sub>K(Ca)</jats:sub>) components of the whole‐cell current.</jats:p></jats:list-item> <jats:list-item><jats:p>In PSS and Cs<jats:sup>+</jats:sup>‐based pipette solution, hypoxia reversibly suppressed <jats:italic>I</jats:italic><jats:sub>Ca</jats:sub> by 30 ± 5% at 0mV.</jats:p></jats:list-item> <jats:list-item><jats:p>When Ba<jats:sup>2+</jats:sup> was used as a charge carrier, the <jats:italic>I</jats:italic><jats:sub>Ba</jats:sub> was suppressed by hypoxia in a potential‐dependent manner, with the maximum of 40 ± 7% at +10mV. Alterations of concentrations of <jats:sc>egta</jats:sc>, GDBβS or ATP in the pipette solution did not change the inhibitory effects of hypoxia on <jats:italic>I</jats:italic><jats:sub>Ca</jats:sub> and <jats:italic>I</jats:italic><jats:sub>Ba</jats:sub>.</jats:p></jats:list-item> <jats:list-item><jats:p>In PSS with 2 mm CaCl<jats:sub>2</jats:sub> replaced by CoCl<jats:sub>2</jats:sub>, hypoxia did not affect the Ca<jats:sup>2+</jats:sup> influx‐independent potassium current.</jats:p></jats:list-item> <jats:list-item><jats:p>In cells voltage clamped at ‐20 mV hypoxia reversibly inhibited the spontaneous transient outward currents.</jats:p></jats:list-item> <jats:list-item><jats:p>The response of high K<jats:sup>+</jats:sup>‐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<jats:sc>m</jats:sc>), while relaxations were unaffected by atropine and guanethidine (10 μ<jats:sc>m</jats:sc>).</jats:p></jats:list-item> <jats:list-item><jats:p>The results show that hypoxia reversibly inhibits <jats:italic>I</jats:italic><jats:sub>Ca</jats:sub> and secondarily suppresses <jats:italic>I</jats:italic><jats:sub>K(Ca)</jats:sub> due to decreased Ca<jats:sup>2+</jats:sup> influx through Ca<jats:sup>2+</jats:sup> channels.</jats:p></jats:list-item> <jats:list-item><jats:p>It is suggested that inhibition of <jats:italic>I</jats:italic><jats:sub>Ca</jats:sub> was responsible for the rapid relaxation, whereas transient contraction may have been due to release of acetylcholine from nerve terminals upon hypoxia.</jats:p></jats:list-item> </jats:list> </jats:p>

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