Effects of ryanodine on tension development in rat aorta and mesenteric resistance vessels

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Abstract
1 The effects of ryanodine on contractile responses dependent either on intracellular Ca2+ release or on extracellular Ca2+ influx were studied in aorta and mesenteric resistance vessels of the rat. 2 In aorta, in the presence of extracellular Ca2+, pretreatment with ryanodine (10−5 m) did not modify contractile responses to noradrenaline (NA) (10−6 m) whereas in the absence of Ca2+, 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 Ca2+ but totally abolished contractile responses to caffeine (10−2 m) in the absence of Ca2+. 4 In K+-depolarized mesenteric resistance vessels, pretreatment with ryanodine (10−5 m) significantly enhanced contractile responses to Ca2+ concentrations higher than 10−4 m and 10−3 m for arteries depolarized with 30 mm and 40 mm K+ respectively. Concentrations of either diltiazem (6 × 10−7 m) or nifedipine (10−8 m) that abolished contractile responses to Ca2+ in depolarized arteries (K+, 40 mm) did not totally inhibit the enhancement of Ca2+-induced contractions obtained in the presence of ryanodine. 5 Ryanodine did not modify the Ca2+ 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 Ca2+ from intracellular stores, resulting in a subsequent reduction of the amplitude of contractions dependent upon intracellular Ca2+ liberation. Furthermore, the ability of sarcoplasmic reticulum to buffer rises in cytoplasmic Ca2+ may be reduced in the presence of ryanodine, thereby accounting for the potentiation of contractile responses to Ca2+ in K+-depolarized mesenteric resistance vessels.