Abstract
In addition to the negative feedback control of transmitter release exterted by the neurotransmitter itself, there are also other substances which may play a modulatory role in autonomic neuro-effector transmissions. Prostaglandins (PGs) belong to this class of substances. This review highlights the action of PGs and indomethacin on adrenergic and cholinergic neuro-effector transmissions in the guinea-pig vas deferens and dog trachea. In the guinea-pig vas deferens, low concentrations of the PGE series markedly suppressed the amplitude of e.j.p. without affecting the membrane potential, input membrane resistance or sensitivity of the smooth muscle cells to noradrenaline. [Ca]0 appeared to counteract the inhibitory action of PGs on the amplitude of e.j.p., indicating that low concentrations of PGs interact with [Ca]0 at the activated nerve terminals. Endogenous PGs may not play, however, a physiological role in the regulation of noradrenaline release, since indomethacin had no effect on the e.j.p. On the contrary, gradual and continuous reduction in the amplitude of e.j.ps was abolished by indomethacin in the dog trachea and e.j.ps with a constant amplitude were recorded. Low concentrations of PGs markedly reduced the amplitude of e.j.ps without affecting membrane properties of the smooth muscle cells. When indomethacin in repeated doses was given, spontaneous coughing and wheezing occurred in half the number of dogs. Endogenous PGs, therefore, probably play an important role in the negative feedback regulation of transmitter release from the cholinergic nerve terminals, in the dog trachea. Topical and species differences in the modulatory role of PGs was discussed.
