Effects of calcium entry blockers, diltiazem, verapamil and nifedipine, were investigated in isolated frog rectus abdominis muscles. Acetylcholine(ACh) and KCI produced concentration-dependent contraction in normal physiological salt solution(NPSS). In 0 Ca²^+-PSS, however, ACh-induced contraction w...
Effects of calcium entry blockers, diltiazem, verapamil and nifedipine, were investigated in isolated frog rectus abdominis muscles. Acetylcholine(ACh) and KCI produced concentration-dependent contraction in normal physiological salt solution(NPSS). In 0 Ca²^+-PSS, however, ACh-induced contraction was significantly weakened and KCl did not alter the basal tension. CaCl₂, did not produce any contraction in NPSS, but elicited dose-dependent contraction in high K^+, 0 Ca²^+-PSS. ACh(35 ,□M)-and KCl(20 mM)-induced tensions were inhibited by diltiazem and nifedipine in a concentration-dependent fashion. Verapamil and nifedipine directly produced contractions in a dose-dependent manner in only NPSS, but diltiazem elicited contractile responses in 0 Ca²^+ -PSS as well as in NPSS. The diltiazem-induced tension was not altered by addition of d-tubocurarine. When nifedipine did not cause any contraction in 0 Ca²^+-PSS, addition of 1.6 mM CaCl₂, to the bath produced a marked contraction. The results suggest that calcium entry blockers directly contract frog rectus abdominis muscle, and inhibit ACh-and KCl-induced tension.
Effects of calcium entry blockers, diltiazem, verapamil and nifedipine, were investigated in isolated frog rectus abdominis muscles. Acetylcholine(ACh) and KCI produced concentration-dependent contraction in normal physiological salt solution(NPSS). In 0 Ca²^+-PSS, however, ACh-induced contraction was significantly weakened and KCl did not alter the basal tension. CaCl₂, did not produce any contraction in NPSS, but elicited dose-dependent contraction in high K^+, 0 Ca²^+-PSS. ACh(35 ,□M)-and KCl(20 mM)-induced tensions were inhibited by diltiazem and nifedipine in a concentration-dependent fashion. Verapamil and nifedipine directly produced contractions in a dose-dependent manner in only NPSS, but diltiazem elicited contractile responses in 0 Ca²^+ -PSS as well as in NPSS. The diltiazem-induced tension was not altered by addition of d-tubocurarine. When nifedipine did not cause any contraction in 0 Ca²^+-PSS, addition of 1.6 mM CaCl₂, to the bath produced a marked contraction. The results suggest that calcium entry blockers directly contract frog rectus abdominis muscle, and inhibit ACh-and KCl-induced tension.
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