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Evoked tensions in rabbit aorta by emptying intracellular Ca2+ stores with cyclopiazonic acid, thapsigargin, and ryanodine

  
@article{APS6212,
	author = {Da-li LUO and Wen-han LI},
	title = {Evoked tensions in rabbit aorta by emptying intracellular Ca2+ stores with cyclopiazonic acid, thapsigargin, and ryanodine},
	journal = {Acta Pharmacologica Sinica},
	volume = {16},
	number = {3},
	year = {2016},
	keywords = {},
	abstract = {AIM: To study the increase of plasma membrane Ca2+ permeability in response to depletion of intracellular Ca2+ stores.
METHODS: In Ca(2+)-free medium, 2 selective inhibitors of sarcoplasmic reticulum (SR) Ca2+ pump ATPase, cyclopiazonic acid (CPA) and thapsigargin (Tha), and an activator of Ca(2+)-induced Ca2+ release channel (CICR), ryanodine (Rya), depleted intracellular Ca2+ stores sensitive to both caffeine and phenylephrine in rabbit aortic rings and caused sustained tensions when Ca2+ reintroduction. These tensions were taken as the increase of plasma Ca2+ permeability by depletion of intracellular Ca2+ stores.
RESULTS: The extracellular Ca(2+)-dependent tensions caused by Tha and Rya 3 mumol.L(-1) and CPA 30 mumol.L(-1) were 0.94, 1.1, and 0.14 g, respectively, and the tension caused by Rya was not inhibited by CPA.
CONCLUSION: (a) Besides the depletion of intracellular Ca2+ stores, an activated state of Ca2+ release channels in SR may also mediate the activation of Ca2+ influx from plasma membrane in rabbit aorta; (b) Rya needs caffeine to fully open CICR channel in SR.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/6212}
}