• Corpus ID: 11518737

[Mechanism of catecholamine release from the sympathetic nerve endings, particularly in its relation tovacetylcholine an experiment on the isolated vas deferens of rats].

@article{Ueba1976MechanismOC,
  title={[Mechanism of catecholamine release from the sympathetic nerve endings, particularly in its relation tovacetylcholine an experiment on the isolated vas deferens of rats].},
  author={Reiko Ueba},
  journal={Nihon yakurigaku zasshi. Folia pharmacologica Japonica},
  year={1976},
  volume={72 1},
  pages={
          127-137
        }
}

• R. Ueba
• Published 1976
• Biology, Chemistry
• Nihon yakurigaku zasshi. Folia pharmacologica Japonica

UNLABELLED
The mechanism of catecholamine (CA) release induced by transmural stimulation (TS) and the participation of acetylcholine (ACh) in this mechanism were studied using isotonic contraction of excised vas defernse of rats. Furthermore, the inhibitory effect of bretylium (Br) on sympathetic activity was observed.

RESULTS
1) The effects of various kinds of drugs on isotonic contractions induced by TS, exogenous ACh and exogenous noradrenaline (NA) were observed with the results shown in Table 1. The following has been concluded: (1) TS-induced contraction is due to stimulation of the endings of hypogastric nerve (sympathetic nerve), resulting in CA release from adrenergic fiber (AF) and ACh release from cholinergic fiber (CF) in this nerve. (2) The participation of ACh is not indispensable in the CA release from AF induced by TS. (3) Endogenous ACh release from CF by TS brings about CA release under eserine application. (4) CA release by exogenous ACh is not inhibited by ganglion blockade, but is inhibited by atropine, indicating the muscarinic receptor to be in AF endings. 2) Br exerted preferentially the irreversible inhibition on CA release from AF rather than that on ACh release from CF, while it caused a mild reversible inhibition on CA release by exogenous ACh. 3) On the TS contraction that had been abolished irreversibly by Br, NA incubation showed a mild lasting recovery, while methamphetamine (MAP) or calcium (Ca) incubation showed a strong lasting recovery. Furthermore, in this recovery of TS contraction, the incubation with NA or MAP exerted only the recovery of CA release while the Ca incubation exerted the recovery of both CA release and ACH release. It would appear that Br blocks both AF and CF by inhibiting the transmitter-releasing action of Ca.