| Abstract
| - Summary. The prostaglandins, a family of widely distributed tissue hormones, play a role in the regulation of many physiological functions in man. Prostaglandins have been shown to influence the release of adrenergic neurotransmitters from nerve endings, possibly by a direct mechanism. They may also modulate the response of target organs to the neurotransmitter. The effects of prostaglandins on autonomic neurotransmission in vitro are frequently different from those observed in the intact organism. Prostaglandins of the E series, PGD2, and the endoperoxides inhibit autonomic neurotransmission in isolated tissues, probably by a presynaptic effect, whereas prostaglandins of the F series, PGA2, and PGB2 appear to have variable effects on norepinephrine release, depending on the concentrations used. Inhibitors of prostaglandin synthesis such as indomethacin or meclofenamate have been observed to increase the release of norepinephrine induced by nerve stimulation in many in vitro perfused organs. High doses of indomethacin, given to conscious rats, caused a significant increase in urinary norepinephrine excretion. However, the observed increase may have been related to toxic effects of indomethacin. In contrast, therapeutic doses of indomethacin have been found to produce a significant decrease in plasma norepinephrine in normal man, mediated probably by a baroreceptor feedback mechanism. The mechanism by which prostaglandins affect norepinephrine release from autonomic nerve endings is incompletely understood. The available evidence suggests that prostaglandins interfere somehow with the stimulus-secretion coupling.
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