1 A study has been made of the pharmacology of the 5‐hydroxytryptamine (5‐HT)‐induced depolarization responses that can be recorded extracellularly from the rat isolated cervical vagus nerve. 2 Phenylbiguanide (PBG) and 2‐methyl‐5‐hydroxytryptamine (2‐methyl‐5‐HT) were found to mimic the effects of 5‐HT on the vagus nerve. Their EC50 values were respectively 2.0 fold and 3.9 fold greater than that of 5‐HT. 3 Metoclopramide behaved as a reversible competitive antagonist of depolarization induced by PBG and 2‐methyl‐5‐HT, with pKB values of 6.48 ± 0.04 and 6.64 ± 0.04, respectively. These agreed well with the pKB value of 6.60 ± 0.04 obtained previously for metoclopramide against 5‐HT on the rat vagus nerve. 5‐HT, PBG and 2‐methyl‐5‐HT had no demonstrable agonist effects at non‐5‐HT receptors on the rat vagus nerve. 4 Tropacaine and m‐chlorophenylpiperazine were found to behave as reversible competitive antagonists of 5‐HT‐induced depolarization of the vagus nerve. The pKB values were 6.29 ± 0.03 and 6.90 ± 0.03, respectively. 5 Quipazine, MDL 72222 and ICS 205–930 were also shown to be effective antagonists of 5‐HT on the vagus nerve. However, although these compounds were highly potent, they all caused a marked concentration‐dependent reduction in the amplitude of the maximum response to 5‐HT. This behaviour was not consistent with a simple reversible competitive mechanism. 6 The results are discussed with reference to the current classification of mammalian peripheral neuronal 5‐HT receptors.
British Journal of Pharmacology – Wiley
Published: Jan 1, 1987
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