Effects of calcium entry blockers on tension development and calcium influx in rat uterus

@article{Granger1986EffectsOC,
  title={Effects of calcium entry blockers on tension development and calcium influx in rat uterus},
  author={S E Granger and Michael Hollingsworth and Arthur Henry Weston},
  journal={British Journal of Pharmacology},
  year={1986},
  volume={87}
}
1 Spontaneous and potassium chloride (KCl)‐induced tension development of strips of whole uterus from the day‐22 pregnant rat was reduced when the tissues were incubated in a calcium ion (Ca2+)‐free medium. 2 Strips of whole uterus, in an initially Ca2+‐free medium, responded to the cumulative addition of Ca2+ with graded phasic tension development and associated rapid electrical discharges. The spasms were inhibited by gallopamil (100 nM) and diltiazem (1 μM). 3 Strips of whole uterus in a… 
Ca(2+)-independent contraction induced by hyperosmolar K(+)-rich solutions in rat uterus.
TLDR
The results suggest that different mechanisms are involved in the responses evoked by isoosmotic and hyperosmotic KCl in the rat uterus, and a component of the contraction induced by hypertonic KCl seems mainly independent of both external and internal Ca2+ and ofhyperosmolar stress.
The spasmogenic action of oxytocin in the rat uterus – comparison with other agonists
TLDR
It is concluded that the phasic component of the response of the uterus to oxytocin and bradykinin is associated with Ca2- influx via voltage‐dependent Ca2+ channels, and the tonic component is due to another mechanism(s) which does not appear to involve Ca2 + influx.
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TLDR
The effects of the flavonoids genistein, kaempferol and quercetin on KCl (60 mM)-induced tonic contraction in rat uterus and their modifications with the inhibitor of cAMP-dependent protein kinases, nifedipine and verapamil and the activator of adenylyl cyclase forskolin were studied.
In vitro effects of calcium entry blockers, chlorpromazine and fenoterol upon human pregnant myometrium contractility
TLDR
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TLDR
It is demonstrated that PAR-2 may actively regulate SMC during pregnancy by modulating Ca( 2+) influx through L-type voltage-gated Ca(2+) channels, and that this increase of I(Ca-L) may be primarily mediated by PLC and PKC activation.
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TLDR
Okadaic acid‐ and nifedipine‐insensitive responses to ouabain, K+‐free and low Na+ solution were enhanced by increasing the extracellular concentration of Ca2+ in the medium and were inhibited in a dose‐dependent manner by amiloride.
Effects of Mn2+ on the responses induced by different spasmogens in the oestrogen-primed rat uterus.
TLDR
Mn2+ enters the cell mainly through nifedipine-insensitive receptor-operated channels and, to a lesser degree, through L-type Ca2+ channels to produce contraction by directly activating the contractile machinery.
Extracellular and intracellular calcium sources mediating contractile responses of smooth muscle in bovine ovarian follicle and ovarian artery.
The relative importance of extracellular and intracellular calcium sources mediating smooth muscle contraction in ovarian follicle and ovarian artery was assessed in experiments on the influence of
CyPPA, a positive modulator of small-conductance Ca(2+)-activated K(+) channels, inhibits phasic uterine contractions and delays preterm birth in mice.
TLDR
Pharmacologic stimulation of myometrial K(Ca)2.2/2.3 channels effectively suppresses Ca(2+)-mediated uterine contractions and delays preterm birth in mice, supporting the potential utility of this approach in tocolytic therapies.
Effect of diphenylhydantoin on drug and calcium induced contractions of isolated rat uterus: a comparative study with nifedipine.
  • J. Calixto
  • Chemistry, Medicine
    General pharmacology
  • 1987
TLDR
The sustained contractions induced by K+, acetylcholine (ACh) and oxytocin (Ot) were inhibited in a concentration-dependent fashion by diphenylhydantoin (DPH) and nifedipine (NIF), suggesting a competitive type of antagonism, between Ca2+ and DPH.
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