To observe calcium utilization mediated by voltage operated-and receptor operated-calcium channels, effect of potassium chloride(KCl) on ACh-induced isolated duodenal contraction was compared with the effect in the
presence of various calcium antagonists
The addition of 16mM KCl produced phasic contraction and it was followed by time-dependent increment of tonic contraction for 2 minutes. However, the tonic contraction significantly decreased at 33mM and 67 mM KCl. By the
presence
of high concentration of KCl, ACh-induced phasic contraction was more inhibited than tonic contraction.
By the presence of nifedipine(8×10-5 mM), KCl-induced phasic and tonic contractions was completely inhibited, whereas ACh-induced phasic and tonic contractions at various concentrations of KCl was little affected.
By the presence of diltiazem(6×10-4 mM), KCl-induced contraction and the ACh-induced contraction were inhibited to same degree.
By presence of verpamil(2×10-5 mM) or cobalt chloride(2.6 mM), KCl-induced contractions were-markedly inhibited. However, the ACh-induced phasic contraction was little affected, otherwise ACh-induced tonic contraction was decreased in
the
presence of cobalt chloride, itself.
These results indicated that high concentrations of KCl(which is related to calcium influx)
produce inhibitory action to ACh-induced contraction, especially phasic contraction(which is related to calcium release).
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