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 arachidonic cascade in muscle damage. We examined the effects of L-type calcium channel antagonists on the release of prostaglandin E(2) (PGE(2)), a bioactive metabolite of arachidonic acid metabolism, from skeletal muscle. The basal release of PGE, was not affected by calcium channel inhibitors, such as nifedipine and verapamil. The release of PGE(2) induced by dinitrophenol, an uncoupler of oxidative phosphorylation, was abolished by nifedipine and verapamil at 50 and 150 mu M, respectively. It was not necessary to include the calcium channel blockers in the medium before or at the time of dinitrophenol stimulation to produce the effect on PGE, release. The release of PGE(2) was prevented for as long as calcium channel blockers were present in the medium after the dinitrophenol stress.