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

Abstract

SUMMARY1. In the glycogen-depleted smooth muscle ofthe guinea-pig taenia coli, application of glucose or fl-hydroxybutyrate (, in the presence of 20 mM-K or carbachol (5 /lM) produced a transient hyperpolarization for about 1 min followed by a sustained depolarization accompanied by spike activity.2. The early hyperpolarization was highly temperature dependent, so that below 30 TC, substrate application produced the depolarization with a delay of approximately 2 min, without a clear preceding hyperpolarization.3. The responses to substrate were not affected by ouabain (10 ftM). 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.4. Verapamil (0-1 ,tM) 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.5. 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 approximately 20 mm. Both the hyperpolarization and the depolarization were not clearly affected by completely replacing Na with choline.6. The results suggest that ATP supplied by the addition of substrate activates some electrogenic pump, probably a Ca pump, causing hyperpolarization, and that ATP also removes the inactivation of Ca conductance with some delay, resulting in an increased depolarization.

Phosphorous compounds studied by 31P nuclear magnetic resonance spectroscopy in the taenia of guinea‐pig caecum.

“…These changes recovered completely on glucose (11-8 mM) readmission. Similar recovery was observed with 11 8 mM-/3-hydroxybutyrate (,f-HB), which is a substrate metabolized directly through oxidative phosphorylation and has been shown to be capable of substituting for glucose in this tissue (Bueding, Biilbring, Gereken, Hawkins & Kuriyama, 1967;Ashoori et al 1984;Takai et al 1985). The tension development caused by excess K+ is known to be reduced by glucose removal, accompanied by depletion of the tissue glycogen (Axelsson, Hogberg & Timms, 1965;Pfaffman, Urakawa & Holland, 1965;Ashoori et al 1984).…”

“…These changes recovered completely on glucose (11-8 mM) readmission. Similar recovery was observed with 11 8 mM-/3-hydroxybutyrate (,f-HB), which is a substrate metabolized directly through oxidative phosphorylation and has been shown to be capable of substituting for glucose in this tissue (Bueding, Biilbring, Gereken, Hawkins & Kuriyama, 1967;Ashoori et al 1984;Takai et al 1985). obtained by accumulating 5000 signals at 0-6 s intervals in a 10 mm tube at a superfusion rate of 6 ml/min.…”

“…Thus, the emphasis of the present experiments was on the comparison with previous metabolic studies on the taenia (Ashoori, Takai, Tokuno & Tomita, 1984;Ishida, Takagi & Urakawa, 1984;Takai, Tokuno & Tomita, 1985). In these studies, recovery of K+ contracture with application of substrates was investigated following glycogen depletion caused by producing K+ contracture in the absence of glucose, and, using a conventional biochemical analysis, some correlation was found between tension development and tissue content of ATP.…”