Effects of agents that modulate potassium permeability on smooth muscle cells of the guinea‐pig basilar artery

Effects of agents that modulate potassium permeability on smooth muscle cells of the guinea‐pig... 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 (10−7‐10−5M), 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 10−4M) 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 appliction of diltiazem (10−5M). 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 (10−6‐10−4M) 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 (10−4M) 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

Effects of agents that modulate potassium permeability on smooth muscle cells of the guinea‐pig basilar artery

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Publisher
Wiley
Copyright
1983 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
DOI
10.1111/j.1476-5381.1983.tb10491.x
Publisher site
See Article on Publisher Site

Abstract

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 (10−7‐10−5M), 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 10−4M) 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 appliction of diltiazem (10−5M). 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 (10−6‐10−4M) 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 (10−4M) 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.

Journal

British Journal of PharmacologyWiley

Published: May 1, 1983

References

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