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