Maintained contractions of rat uterine smooth muscle incubated in a Ca²⁺‐free solution

Abstract

1The effects of acetylcholine (10-4 M), prostaglandin E2 (10-6 M), vanadate (5 x 10-4M) and fluoride (10-2 M) have been studied on the mechanical and electrical activities of rat myometrial strips perfused in Ca2+-free EGTA-containing solutions. (fluoride) or Ca2+ release from an intracellular store. This latter mechanism would include both pharmacomechanical (prostaglandin E2, vanadate) and electromechanical (acetylcholine) coupling.

Properties of intracellular calcium stores in pregnant rat myometrium

“…Oxytocin and acetylcholine have been shown to induce repetitive contractions of rat myometrium in Ca2 '-free solution (Mironneau et al, 1984;Ashoori et al, 1985). It has also been suggested that hydrolysis of PIP2 might play a role in transferring the activation of muscarinic and oxytocin receptors to the sarcoplasmic reticulum in human and guinea-pig myometrium (Schrey et al, 1986;Marc et al, 1986), and InsP3 was reported to release Ca2+ from microsomes from the sarcoplasmic reticulum of bovine pregnant uteri (Carsten & Miller, 1985).…”

“…The activator Ca2+ is either released from intracellular stores (mainly from sarcoplasmic reticulum), or extracellular Ca2 + enters through the Ca2 +-channels of the plasma membrane. Because acetylcholine (ACh) elicits a phasic contraction of myometrium in Ca2+-free solution containing EGTA, it has been proposed that in this tissue agonists can release Ca2+ from intracellular stores (Mironneau et al, 1984;Izumi, 1985).…”

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

“…Several agents are, nevertheless, capable of initiating tension development in uteri bathed in Ca2'-free media (Mironneau et al, 1984) although these mechanical responses are small relative to those obtained when physiological concentrations of Ca2+ are present. Thus, the uterus is generally classed as a tissue in which tension development is largely dependent on extracellular Ca2+ rather than on intracellular Ca2+ pools (Bolton, 1979 ('calcium antagonists') since these drugs are considered to act by reduction of Ca2" entry through voltage-operated Ca2" channels (Bolton, 1979;Nayler & Horowitz, 1983).…”

Comparative effects of Mg, Ca, Sr, and verapamil on the uterine longitudinal muscle of spayed and estrogen-treated rats.

“…With some exceptions such as Ca-free contraction of uterine muscle (SAKAI et a!., 1981;MIRONNEAU et al, 1984;AsxooRl et at.,1985), it is generally accepted that smooth muscle contraction is a function of intracellular Ca concentration (ENDO et al,1977;OCHIAI et a!.,1981). Intracellular Ca of smooth muscles is by some means, e.g.…”