Premium
[Ca 2+ ] i ‐sensitive, IP 3 ‐independent Ca 2+ influx in smooth muscle of rat vas deferens revealed by procaine
Author(s) -
Khoyi Mohammad A.,
Dalziel Hugh H.,
Zhang Lubo,
Bjur Richard A.,
Gerthoffer William T.,
Buxton Iain L.O.,
Westfall David P.
Publication year - 1993
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.1476-5381.1993.tb13968.x
Subject(s) - procaine , vas deferens , inositol , chemistry , inositol trisphosphate , endocrinology , medicine , calcium , inositol phosphate , contraction (grammar) , phentolamine , intracellular , biophysics , propranolol , biology , pharmacology , biochemistry , receptor
1 The actions of procaine (10 m m ) on noradrenaline‐induced effects on 45 Ca‐influx, 45 Ca‐efflux, 45 Ca‐content, total inositol phosphates, inositol‐1,4,5‐trisphosphate, and contractile status of the rat vas deferens were examined. 2 Noradrenaline alone had no effect on 45 Ca‐influx or 45 Ca‐content, but released Ca 2+ from intracellular stores as indicated by an increased 45 Ca‐efflux and increased total inositol phosphates, specifically inositol‐1,4,5‐trisphosphate, leading to contraction of the rat vas deferens. 3 Noradrenaline, in the presence of 10 m m procaine, increased 45 Ca‐influx and 45 Ca‐content. Procaine blocked the noradrenaline‐induced 45 Ca‐efflux, the increase in total inositol phosphates, the increase in inositol‐1,4,5‐trisphosphate, and contraction. 4 The noradrenaline‐induced increase in 45 Ca influx which was observed in the presence of procaine was abolished by phentolamine and nifedipine but was not altered significantly by propranolol suggesting that, in the presence of procaine, noradrenaline activates dihydropyridine‐sensitive calcium channels through α‐adrenoceptors. 5 These findings indicate that, in the rat vas deferens, noradrenaline induces contraction by releasing intracellularly stored Ca 2+ . The effects of procaine appear to be due to its ability to block the release of Ca 2+ from intracellular stores. Furthermore, the simultaneous increase in 45 Ca influx and inhibition of inositol‐1,4,5‐trisphosphate formation in tissues treated with procaine plus noradrenaline indicates that Ca 2+ influx is independent of inositol‐1,4,5‐trisphosphate formation.