RESUMEN
The objective of the present study was to evaluate the electrophysiological effects of the peptide somatostatin (SST) at the supraventricular level in isolated guinea hearts. ECG recording from isolated hearts perfused by the Langendorff method i9ndicating that 1.0 uM SST induced a decrease in heart rate from 174 ñ 15 to 157 ñ 9 bpm (N=6, P<0.05), blocked AV conductio9n (the PR interval increased from 92 ñ 11 ms to 106 ñ 5 ms, N+5, P<0.05) and increased the QTc interval from 210 ñ 0 to 232 ñ 4 ms (N+5, P<0.05). The supraventricular effect of SST, particulary upon the AV conduction , were potentiated by a reduction in calcium concentration from 2.5 to 0.5 mM in the perfusing solution. Thus, 1.0 uM SST induced 2nd degree AV conduction block progressing to AV dissociation in 75% of thye hearts in the low calcium medium instead of the first degree conduction block observed in all hearts in normal calcium medium. His bundle electrogram evidence a complete A-H dissociation withouth significant change in the H-V interval and microelectrode studies showed a complete abolition of the AV node action potential in the presence of 1.0 uM SST. Both results demonstrate that the site of AV conduction block induced by SST is at the AV node. All the supraventricular effects of SST were transitory, subsiding within abouth 10 min of hormone exposition, showing desensitization. The effects of somatostatin here described were not blocked by 10 uM atropine, indicating that they are not mediated by muscarinic receptors. These data provide a direct electrophysiological demonstration of the supraventricular effects of SST, and suggest that this peptide decreases calcium influx during the action potential