Activities of prostaglandins and prostaglandin endoperoxides at adrenergic neuroeffector junctions.

The results presented in this paper indicate that: 1. The prostaglandin synthesis inhibitor, indomethacin, increases noradrenaline turnover in a variety of rat organs. This observation increases the probability that prostaglandins are involved in the control of adrenergic neurotransmission in vivo. 2. Administration of endoperoxides inhibits the release of noradrenaline from adrenergic nerve terminals. The effect can be explained, however, at least in part, by formation of degradation products, presumably mainly prostaglandin E2. 3. Prostaglandin F2 alpha enhances smooth muscle responses to adrenergic nerve stimulation in rabbit heart and guinea pig vas deferens. These actions must be considered prostjunctional, since the release of noradrenaline is unchanged or depressed.