Vagal stimulation and somatostatin potentiate cardiac vagal action in the toad, Bufo marinus.
Cholinergic postganglionic neurones of the cardiac vagus in the toad, Bufo marinus, have been shown to contain the peptide somatostatin (SOM), which causes direct negative inotropic and chronotropic effects on the heart. In anaesthetised toads, high frequency stimulation (10 Hz) of cardiac vagus nerves results in prolonged cardiac slowing and potentiation of the cardiac slowing measured in response to a train of vagal stimuli at low frequency. Intravenous administration of the tetradecapeptide form of SOM also results in prolonged cardiac slowing and potentiation of cardiac vagal action. Effects on heart rate of small bolus doses of acetylcholine (ACh) were unaltered by administration of SOM, at the same time as cardiac vagal slowing was enhanced. It is suggested that SOM is released from vagal nerve endings by high frequency stimulation and enhances cardiac vagal action by a presynaptic mechanism.
School of Physiology and Pharmacology, University of New South Wales, Kensington, Sydney, Australia.
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Courtice
D000818:Animals; D002024:Bufo marinus; D004558:Electric Stimulation; D006321:Heart / Q000187:drug effects* / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects; D013004:Somatostatin / Q000494:pharmacology*; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*
D013004:Somatostatin