Muscarinic antagonists potentiate beta-adrenergic relaxation of the sphincter by affecting the apparent potency of beta-adrenergic agonists and not by antagonizing the intrinsic tonus produced by endogenously released acetylcholine.
Bovine iris sphincter in vitro responded to L Ladrenergic stimulation with pronounced relaxation (EC SH of isoproterenol = 0.3 nM), which was potentiated by the cAMP phosphodiesterase inhibitor, isobutylmethylxanthine, and mimicked by the adenylyl cyclase activator, forskolin. The L L I /L L P antagonist, propranolol, exhibited low potency with calculated
Helium-neon low-energy laser (LEL) irradiation, known for its therapeutic effects in arthritis, wound healing, and muscular strain, was applied to eyes of rats that had sustained an optic nerve crush injury. Crush injury to the optic nerve resulted in a long-lasting in vitro elevation of prostaglandin E2 (PGE2) production (1.8-3.9-fold above control values during the 12 day study period). LEL irradiation per se had no effect in vitro on PGE2 production by the optic nerve; however, LEL irradiation of eyes with crushed optic nerve inhibited the enhanced production of PGE2 and leukotriene B4 in vitro by 55% and 75% during the late and immediate phase after trauma, respectively. Our findings of the suppressive effect of LEL irradiation on arachidonic acid metabolism are reminiscent of the actions of steroidal and nonsteroidal anti-inflammatory drugs, and might indicate, for the first time, the possible biochemical mechanisms associated with the clinical anti-inflammatory effects of LEL irradiation.
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