Effects of readmission of substrate on the membrane potential in glycogen‐depleted guinea‐pig taenia coli.

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Abstract
In the glycogen-depleted smooth muscle of the guinea-pig tenia coli, application of glucose or .beta.-hydroxybutyrate (.beta.-HB) in the presence of 20 mM-K or carbachol (5 .mu.M) produced a transient hyperpolarization for .apprx. 1 min followed by a sustained depolarization accompanied by spike activity. The early hyperpolarization was highly temperature dependent, so that < 30.degree. C, substrate application produced the depolarization with a delay of .apprx. 2 min, without a clear preceding hyperpolarization. The responses to substrate were not affected by ouabain (10 .mu.M). Readmission of K after a treatment with K-free solution for 10 min caused a transient hyperpolarization only in the presence of substrate. This hyperpolarization was abolished by ouabain. Verapamil (0.1 .mu.M) blocked the substrate-induced depolarization, revealing an underlying slow hyperpolarization. Removal of Ca abolished both the hyperpolarization and depolarization caused by substrate application, but the hyperpolarization disappeared much more slowly than the depolarization. Removal of the external K had little effect on the substrate-induced hyperpolarization, but the hyperpolarization induced by substrate application was increased when the external K was increased up to .apprx. 20 mM. Both the hyperpolarization and the depolarization were not clearly affected by completely replacing Na with choline. Apparently, ATP supplied by the addition of substrate activates some electrogenic pump, probably a Ca pump, causing hyperpolarization; ATP also removes the inactivation of Ca conductance with some delay, resulting in an increased depolarization.