A role for voltage‐gated, but not Ca²⁺‐activated, K⁺channels in regulating spontaneous contractile activity in myometrium from virgin and pregnant rats

Jan 18, 2006British journal of pharmacology

Voltage-controlled potassium channels, but not calcium-activated ones, influence natural muscle contractions in the womb of virgin and pregnant rats

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Abstract

Inhibition of BK(Ca) channels did not significantly affect contractility in myometrial strips from nonpregnant or pregnant rats.

4-aminopyridine (4-AP) caused concentration-dependent increases in mean integral tension (MIT) in myometrium across all groups.
Tetraethylammonium (TEA) significantly increased MIT in myometrium from nonpregnant and mid- to late pregnant rats, but not in early pregnant rats.
TEA and 4-AP continued to increase MIT even after treatment with high concentrations of penitrem A or a mixture of other inhibitors in nonpregnant rats.
BK(Ca) channels may not play a significant role in regulating basal rhythmicity in rat myometrium.
K(V) channels appear to be crucial for regulating basal contractility, particularly during mid- and late pregnancy.

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The roles of voltage-gated (K(V)) and large conductance Ca2+-activated K+ (BK(Ca)) channels in regulating basal contractility in myometrial smooth muscle are unresolved. The aim of this study was to determine the effects of inhibition of these channels on spontaneous rhythmic contraction in myometrial strips from four groups of rats: nonpregnant and during early (day 7), mid- (day 14), and late (day 21) pregnancy. BK(Ca) channels were inhibited using iberiotoxin (1-100 nM), paxilline (1-10 microM) or penitrem A (1-500, or 3000 nM); K(V) channels were inhibited using tetraethylammonium (TEA; 1-10 mM) and/or 4-aminopyridine (4-AP; 1-5 mM). Contractility was assessed as mean integral tension (MIT). Time/vehicle controls were also performed. None of the selective BK(Ca) channel inhibitors significantly affected contractility in myometrial strips from either nonpregnant or pregnant animals. 4-AP caused concentration-dependent increases in MIT in myometrium in all four groups. TEA (5 and 10 mM) significantly increased MIT in myometrium from nonpregnant, and mid- and late pregnant rats, but not in myometrium from early pregnant rats. TEA and 4-AP still caused an increase in MIT following treatment with 3000 nM penitrem A or a combination of propranolol, phentolamine, atropine (all 1 microM) and capsaicin (10 microM) in myometrial strips from nonpregnant rats. These results indicate that whereas BK(Ca) channels play little or no part in controlling basal rhythmicity in rat myometrium, K(V) channels appear to play a crucial role in this regard, especially during mid- and late pregnancy.

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A role for voltage‐gated, but not Ca²⁺‐activated, K⁺channels in regulating spontaneous contractile activity in myometrium from virgin and pregnant rats

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