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Effects of ryanodine on tension development in rat aorta and mesenteric resistance vessels
Author(s) -
JulouSchaeffer G.,
Freslon J.L.
Publication year - 1988
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.1476-5381.1988.tb11682.x
Subject(s) - ryanodine receptor , mesenteric arteries , extracellular , medicine , contraction (grammar) , caffeine , endocrinology , chemistry , vascular smooth muscle , muscle contraction , biology , calcium , artery , biochemistry , smooth muscle
1 The effects of ryanodine on contractile responses dependent either on intracellular Ca 2+ release or on extracellular Ca 2+ influx were studied in aorta and mesenteric resistance vessels of the rat. 2 In aorta, in the presence of extracellular Ca 2+ , pretreatment with ryanodine (10 −5 m ) did not modify contractile responses to noradrenaline (NA) (10 −6 m ) whereas in the absence of Ca 2+ , pretreatment with ryanodine reduced to about 25% the contractile response to NA (10 −6 m ) and totally abolished the transient contraction elicited by caffeine (5 × 10 −2 m ). 3 In mesenteric resistance vessels, ryanodine (10 −5 m ) had no effects on NA (10 −5 m )‐induced tension in the presence of extracellular Ca 2+ but totally abolished contractile responses to caffeine (10 −2 m ) in the absence of Ca 2+ . 4 In K + ‐depolarized mesenteric resistance vessels, pretreatment with ryanodine (10 −5 m ) significantly enhanced contractile responses to Ca 2+ concentrations higher than 10 −4 m and 10 −3 m for arteries depolarized with 30 m m and 40 m m K + respectively. Concentrations of either diltiazem (6 × 10 −7 m ) or nifedipine (10 −8 m ) that abolished contractile responses to Ca 2+ in depolarized arteries (K + , 40 m m ) did not totally inhibit the enhancement of Ca 2+ ‐induced contractions obtained in the presence of ryanodine. 5 Ryanodine did not modify the Ca 2+ concentration‐effect relationships in mesenteric resistance vessels exposed to NA or arginine vasopressin. 6 These data are consistent with the hypothesis that ryanodine induces a release of Ca 2+ from intracellular stores, resulting in a subsequent reduction of the amplitude of contractions dependent upon intracellular Ca 2+ liberation. Furthermore, the ability of sarcoplasmic reticulum to buffer rises in cytoplasmic Ca 2+ may be reduced in the presence of ryanodine, thereby accounting for the potentiation of contractile responses to Ca 2+ in K + ‐depolarized mesenteric resistance vessels.