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. Cardi ac responses attributed to the release of somatostatin are profound br adycardia, and potentiation of cardiac vagal action by increased acety lcholine 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 card iac vagal action was abolished after a 1-hour period of repetitive vag al stimulation. In the presence of atropine, increases in pulse interv al recorded in response to vagal stimulation at various frequencies fo r 2 min each, were significantly reduced after the hour of repetitive stimulation. Potentiation of cardiac vagal action and increases in bas eline pulse interval were recorded also in response to intravenous inj ection of exogenous somatostatin. These responses were not significant ly 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 neuro peptide somatostatin in the vagal nerve endings.