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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Department of Pharmacology, University of Kiel, Fed. Rep. Germany.

Gen Pharmacol. 1992 May;23(3):403-8. doi: 10.1016/0306-3623(92)90102-p.

In guinea-pig Langendorff hearts, the negative inotropic effect of the calcium antagonist gallopamil is shifted by 15-fold to the left, when the extracellular K(+)-concentration is raised from 2.7 to 8.1 mM. 2. In papillary muscles, the ability of gallopamil to shorten the action potential (AP) markedly depends on K+: 100-fold lower gallopamil concentrations were required at 10.8 mM, compared to 2.7 mM. 3. In isolated myocytes, a change in the holding potential from -90 to -70 mV displaces the gallopamil dose-response curve to block Ca2+ currents leftward by only 6-fold. 4. Tetraethylammonium (TEA, 10 mM) mimics the mitigating effect of low K+ on the gallopamil-induced AP-shortening. Hence, the K(+)-dependence of gallopamil may be comprised of modulation of Ca(2+)-channel and K(+)-channel blocking effects.

在豚鼠离体心脏Langendorff灌流模型中，当细胞外钾离子浓度从2.7 mM升高到8.1 mM时，钙拮抗剂加洛帕米的负性肌力作用向左偏移15倍。2. 在乳头肌中，加洛帕米缩短动作电位（AP）的能力显著依赖于钾离子：与2.7 mM相比，在10.8 mM时所需的加洛帕米浓度低100倍。3. 在分离的心肌细胞中，钳制电位从-90 mV变为-70 mV时，加洛帕米阻断钙电流的剂量反应曲线仅向左偏移6倍。4. 四乙铵（TEA，10 mM）模拟低钾对加洛帕米诱导的动作电位缩短的减轻作用。因此，加洛帕米的钾离子依赖性可能由钙通道和钾通道阻断作用的调节组成。

Department of Pharmacology, University of Kiel, Fed. Rep. Germany.

Gen Pharmacol. 1992 May;23(3):403-8. doi: 10.1016/0306-3623(92)90102-p.

In guinea-pig Langendorff hearts, the negative inotropic effect of the calcium antagonist gallopamil is shifted by 15-fold to the left, when the extracellular K(+)-concentration is raised from 2.7 to 8.1 mM. 2. In papillary muscles, the ability of gallopamil to shorten the action potential (AP) markedly depends on K+: 100-fold lower gallopamil concentrations were required at 10.8 mM, compared to 2.7 mM. 3. In isolated myocytes, a change in the holding potential from -90 to -70 mV displaces the gallopamil dose-response curve to block Ca2+ currents leftward by only 6-fold. 4. Tetraethylammonium (TEA, 10 mM) mimics the mitigating effect of low K+ on the gallopamil-induced AP-shortening. Hence, the K(+)-dependence of gallopamil may be comprised of modulation of Ca(2+)-channel and K(+)-channel blocking effects.

在豚鼠离体心脏Langendorff灌流模型中，当细胞外钾离子浓度从2.7 mM升高到8.1 mM时，钙拮抗剂加洛帕米的负性肌力作用向左偏移15倍。2. 在乳头肌中，加洛帕米缩短动作电位（AP）的能力显著依赖于钾离子：与2.7 mM相比，在10.8 mM时所需的加洛帕米浓度低100倍。3. 在分离的心肌细胞中，钳制电位从-90 mV变为-70 mV时，加洛帕米阻断钙电流的剂量反应曲线仅向左偏移6倍。4. 四乙铵（TEA，10 mM）模拟低钾对加洛帕米诱导的动作电位缩短的减轻作用。因此，加洛帕米的钾离子依赖性可能由钙通道和钾通道阻断作用的调节组成。