Cardiac vagal effects in the toad are attenuated by repetitive vagal stimulation.

The neuropeptide, somatostatin is co-localised with acetylcholine and galanin in cardiac vagal nerve fibres in the toad, Bufo marinus. Cardiac responses attributed to the release of somatostatin are profound bradycardia, and potentiation of cardiac vagal action by increased acetylcholine release. Cardiac slowing in response to a standard electrical stimulus applied to the vagus (1-2 Hz for 10 s) was potentiated after a 2 min high frequency stimulation (10 Hz). This potentiation of cardiac vagal action was abolished after a 1-hour period of repetitive vagal stimulation. In the presence of atropine, increases in pulse interval recorded in response to vagal stimulation at various frequencies for 2 min each, were significantly reduced after the hour of repetitive stimulation. Potentiation of cardiac vagal action and increases in baseline pulse interval were recorded also in response to intravenous injection of exogenous somatostatin. These responses were not significantly different after the hour of repetitive stimulation. It is concluded that attenuation of the cardiac responses described after the hour of repetitive stimulation is due to depletion of the stores of the neuropeptide somatostatin in the vagal nerve endings.