These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Effects of ryanodine on tension development in rat aorta and mesenteric resistance vessels. Author: Julou-Schaeffer G, Freslon JL. Journal: Br J Pharmacol; 1988 Oct; 95(2):605-13. PubMed ID: 3228676. Abstract: 1. The effect 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 x 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 x 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.[Abstract] [Full Text] [Related] [New Search]