ArticlePflugers Archiv : European journal of physiology1992
Properties of the inactivating outward current in single smooth muscle cells isolated from the rat anococcygeus.
Article in Pflugers Archiv : European journal of physiology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Electrophysiology of Ctenophore Smooth Muscle.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Heterogeneous expression of transient outward currents in smooth muscle cells of the mouse small intestine.The Journal of physiology · 2002Article
- Inhibition of capacitative calcium entry is not obligatory for relaxation of the mouse anococcygeus by the NO/cyclic GMP signalling pathway.British journal of pharmacology · 2001Article
- Regulation of smooth muscle delayed rectifier K+ channels by protein kinase A.Pflugers Archiv : European journal of physiology · 1996Article
- Two distinct membrane currents activated by cyclopiazonic acid-induced calcium store depletion in single smooth muscle cells of the mouse anococcygeus.British journal of pharmacology · 1996Article
- Multiple components of delayed rectifier K+ current in canine colonic smooth muscle.The Journal of physiology · 1995Article
- Pharmacology of a cloned potassium channel from mouse brain (MK-1) expressed in CHO cells: effects of blockers and an 'inactivation peptide'.British journal of pharmacology · 1993Article
- Properties of the inactivating outward current in single smooth muscle cells isolated from the rat anococcygeus.Pflugers Archiv : European journal of physiology · 1992Article
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2 authors.
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Abstract
The properties of the voltage- and time-dependent outward current in single smooth muscle cells isolated from the rat anococcygeus were studied. The outward current was activated by depolarizations to membrane potentials positive to -40 mV. Activation followed third order kinetics; at +20 mV, the time for the current to reach half its maximal amplitude was around 55 ms. The current inactivated with a time course that could best be described by a single exponential with a time constant around 1500 ms. The steady-state inactivation curve was voltage dependent over the range -110 to -30 mV, with a half-inactivation point of -67 mV. Recovery from inactivation followed an exponential time course with a time constant of around 770 ms at -90 mV. Deactivating tail current analysis revealed that a 10-fold change in the extracellular potassium ion concentration resulted in a 42 mV change in the reversal potential of the current. The current was blocked by 4-aminopyridine, tetraethylammonium, quinine and verapamil with IC50's--the concentrations producing 50% inhibition of the peak current--of 2 mM, 4 mM, 12 microM and 20 microM respectively. The current was not blocked by Toxin I (100 nM) or glibenclamide (10 microM). The current was still present in cells containing 5 mM EGTA; in these cells, replacing extracellular calcium with cadmium depressed the peak current by around 12%. This could be explained, at least in part, by a negative shift in the voltage dependence of inactivation.
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