The inhibitory effects of frusemide on Ca2+ influx pathways associated with oxytocin-induced contractions of rat myometrium.

Oct 1, 1995General physiology and biophysics

Frusemide’s blocking of calcium entry linked to oxytocin-triggered contractions in rat uterine muscle

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Abstract

Oxytocin at 25 mumol/l induces both phasic and tonic contractions in isolated myometrial strips from estradiol-dominated rats.

Contractions appear to be linked to Ca2+ release from internal stores in a Ca(2+)-free medium.
Frusemide does not impact contractions from Ca2+ release but inhibits those resulting from increased Ca2+ influx.
The effects of frusemide mimic the absence of Ca2+ in the medium, suggesting it blocks oxytocin-induced Ca2+ influx.
Frusemide reduces the amplitude of KCl-induced contractions by approximately 34%, which is concentration-dependent.
The reduction in KCl-induced contraction could be partly countered by dibutyryl-cAMP, indicating a role of cAMP in modulating Ca2+ influx.

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Contractile responses induced by 25 mumol/l oxytocin in myometrial strips isolated from the uterus of estradiol-dominated rats comprised both phasic and tonic components. In a Ca(2+)-free medium (containing 0.1 mmol/l EGTA and no added Ca2+), the oxytocin-induced contractions seemed to be associated with Ca2+ release from intracellular stores. Frusemide, known to lower the cAMP level in the rat myometrium, did not affect the responses due to Ca2+ release but inhibited those mediated through an acceleration of the Ca2+ influx. The permanent presence of frusemide (1.5 mmol/l) in the CaCl2-containing medium influenced the oxytocin-induced responses in the same manner as did omission of Ca2+ from the medium. The frusemide-sensitive component of the responses to oxytocin was superimposed on a persistent contraction caused by KCl depolarization, suggesting that frusemide completely inhibited the oxytocin-induced Ca2+ influx. At the same time, frusemide moderately (by only 34 +/- 7%) decreased the amplitude of the KCl-induced contracture. This decrease varied with the frusemide concentration, and could be partly prevented by addition of dibutyryl-cAMP; i.e. probably, it was mediated by an inhibition of voltage-gated Ca2+ influx due to a decrease in the intracellular cAMP level. The data presented seem to suggest that in the rat myometrium exposed to oxytocin (25 mumol/l) both voltage-gated and receptor-operated Ca2+ entries are regulated by cAMP-dependent protein kinases.

The inhibitory effects of frusemide on Ca2+ influx pathways associated with oxytocin-induced contractions of rat myometrium.

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