Abstract
Evidence from our laboratory shows that peroxides can alter both adrenergic neurosecret ion and postjunctional responses of the bovine iris to pharmacological agents. Purpose. To examine the role of prostaglandins in peroxide-induced alteration of both neurotransmitter release from sympathetic nerves and postjunctional responses of the bovine iris to muscarinic agonists. Mgthods. Isolated hemi-iris strips from bovine eves were prepared for in vitro studies of [3H]-norepinephrine ([3H]NE) release using the superfusion method or for measurement of isometric contractile tension using a Digi-Med Tissue Force Analyzer 200. Results. The cyclooxygenase inhibitor, flurbiprofen (FBF, 10 μM) partially prevented the enhancement of field-stimulated [JH]NE release evoked bv H2O2 (0.3 - 1 mM) and cumene hydroperoxide (cuOOH, 0.03 -0.1 mM). FBF (10 μM) treatment also prevented the attenuation of carbachol contractions caused by H2O2 (0.1 - 1 mM) and cuOOH (0.3 - 1 mM). For instance, H2O2 (0.3 m M)-induced maximal attenuation of carbachol contractions was increased from 54 ± 9% in the absence, to 93 ± 5% in the presence of FBF. Conclusion. Intramurally-generated prostaglandins may be involved in the effects caused by peroxides on sympathetic neurotransmission and on postjunctional responses of the bovine iris to muscarinic agonists.