EFFECTS OF CALCIUM-CHANNEL ANTAGONISTS ON THE RELEASE OF PROSTAGLANDIN E(2) FROM METABOLICALLY STRESSED MUSCLE

Calcium influx plays a critical role in the activation of the arachido nic cascade in muscle damage. We examined the effects of L-type calciu m channel antagonists on the release of prostaglandin E(2) (PGE(2)), a bioactive metabolite of arachidonic acid metabolism, from skeletal mu scle. The basal release of PGE, was not affected by calcium channel in hibitors, such as nifedipine and verapamil. The release of PGE(2) indu ced by dinitrophenol, an uncoupler of oxidative phosphorylation, was a bolished by nifedipine and verapamil at 50 and 150 mu M, respectively. It was not necessary to include the calcium channel blockers in the m edium before or at the time of dinitrophenol stimulation to produce th e effect on PGE, release. The release of PGE(2) was prevented for as l ong as calcium channel blockers were present in the medium after the d initrophenol stress.