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Effects of calcium entry blockers on tension development and calcium influx in rat uterus
Author(s) -
Granger Susan E.,
Hollingsworth M.,
Weston A.H.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb10166.x
Subject(s) - gallopamil , cinnarizine , diltiazem , nifedipine , calcium , verapamil , chemistry , endocrinology , medicine , uterus , pharmacology , chromatography
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 (Ca 2+ )‐free medium. 2 Strips of whole uterus, in an initially Ca 2+ ‐free medium, responded to the cumulative addition of Ca 2+ 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 depolarizing (40 mM K + ) medium, which was initially Ca 2+ ‐free, responded to the cumulative addition of Ca 2+ with graded tonic tension development without associated electrical discharges. These spasms were inhibited by calcium entry blockers with a rank order of potency of nifedipine = gallopamil > diltiazem > cinnarizine. 4 KCl‐induced tension development in endometrium‐free uterine strips was antagonized by calcium entry blockers with a rank order of potency of nifedipine > gallopamil > diltiazem > cinnarizine. 5 Ca 2+ influx into endometrium‐free uterine strips was assessed by means of the lanthanum method'. KCl induced a concentration‐dependent increase in 45 Ca 2+ influx which was suppressed or abolished by nifedipine (2.5 nM), gallopamil (100 nM), diltiazem (500 nM) or cinnarizine (5 μM). 6 It is concluded that spontaneous and KCl‐induced tension development of rat uterus involves Ca 2+ influx from the extracellular medium into the myometrial cell. These results support the hypothesis that nifedipine, gallopamil, diltiazem and cinnarizine inhibit Ca 2+ ‐ and KCl‐induced tension development of rat uterus by reduction of Ca 2+ influx.