Effects of agents that modulate potassium permeability on smooth muscle cells of the guinea-pig basilar artery.
1 Effects of various chemical agents, with known actions on K-permeability, on the membrane potential, membrane resistance and spike activity of smooth muscle cells of the guinea-pig basilar artery were investigated using the microelectrode method. The K-permeability suppressing agents procaine, tetraethylammonium (TEA), 4-aminopyridine (4-AP), and the K-permeability increasing agents acetylcholine (ACh), caffeine and 2-nicotinamidoethyl nitrate (2-NN) were used.2 The mean resting membrane potential of smooth muscle cells was -50.6 mV and was electrically quiescent. The maximum slope of the membrane depolarization produced by a ten fold increase in [K](o) plotted on a log scale was 42 mV. The contribution of the Na-K pump mechanism to the membrane potential was apparent, i.e. the maximum hyperpolarization induced by activation of the Na-K pump was -71 mV. This hyperpolarization ceased following application of ouabain. Reduction in the [Na](o) slightly hyperpolarized the membrane.3 TEA (1-10 mM) and procaine (0.3-10 mM) depolarized the membrane dose-dependently, and increased the membrane resistance. TEA markedly inhibited and procaine slightly inhibited rectification of the membrane.4 Caffeine had dual actions on the membrane potential, i.e. a low concentration (below 1 mM) hyperpolarized the membrane and reduced the membrane resistance, while increased concentrations (above 1 mM) transiently hyperpolarized, and then depolarized the membrane with an increase in the membrane resistance.5 ACh hyperpolarized the membrane dose-dependently (10(-7)-10(-5)M), and reduced the membrane resistance. The hyperpolarizing action of ACh did not persist and even in the presence of ACh, the membrane was repolarized to near the control level.6 2-NN (up to 10(-4)M) and 4-AP (up to 1 mM) did not modify the membrane potential or the membrane resistance.7 TEA (10 mM) generated a spike either spontaneously or by application of electrical stimulation and the spike was preceded or followed by slow oscillatory potential changes. These potential changes ceased with application of diltiazem (10(-5)M).8 Low concentrations of procaine (below 1 mM) accelerated but high concentrations (5-10 mM) inhibited the spike generation in the presence of 10 mM TEA. Low concentrations of caffeine (below 1 mM) inhibited the spike generation and higher concentrations (above 1 mM) of caffeine accelerated the spike generation in the presence of 10 mM TEA. ACh (10(-6)-10(-4)M) consistently inhibited the spike generation, with 10 mM TEA pretreatment.9 4-AP (1 mM) did not modify the membrane potential yet accelerated the spike generation, in the presence of 10 mM TEA. 2-NN (10(-4)M) had no effect on the spike evoked in the presence of 10 mM TEA.10 The results show that the low membrane potential in smooth muscle cells of the guinea-pig basilar artery is mainly due to the low permeability of the membrane to K ion, presumably due to the lack of a K channel sensitive to 2-NN and 4-AP. Similarities and differences between this vascular tissue and other regions are also discussed.
D015761:4-Aminopyridine; D000109:Acetylcholine / Q000494:pharmacology; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D001488:Basilar Artery / Q000378:metabolism; D002110:Caffeine / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism; D010539:Permeability; D011188:Potassium / Q000378:metabolism*; D011343:Procaine / Q000494:pharmacology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D000631:Aminopyridines; D013757:Tetraethylammonium Compounds; D002110:Caffeine; D011343:Procaine; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D004110:Diltiazem; D000109:Acetylcholine; D011188:Potassium