Glucagon: Present status in cardiovascular disease

The actions of pancreatic glucagon, a known hyperglycemic, hypoaminoacidemic, and lipolytic agent, have received recent attention because of a variety of effects mediated by increases in cyclic AMP concentrations. Studies in the dog demonstrated the positive inotropic and chronotropic actions of glucagon, unaltered by reserpine, insulin, or propranolol. Enhanced contractility was additive with that of the digitalis preparations but did not produce undesirable arrhythmias. The ability of glucagon to increase contractility was attenuated with longer duration of experimental congestive heart failure, thus implying greater effectiveness in acute pathology. In man, variables dependent upon contractility are correspondingly enhanced with the use of glucagon. Current evidence suggests glucagon is a secondary coronary vasodilator and lowers renal vascular resistance as well. Restored blood pressure and urine output accompanying clinical improvement have been noted as a result of continuous glucagon therapy in patients with early congestive heart failure, cardiogenic shock, myocardial infarction, and in low output syndromes following open heart surgery. Glucagon appears to activate adenyl cyclase to increase cycliC AMP levels, which in tum enlarges the intracellular calcium pool. Thus, according to current excitation‐contraction theories, an increase in contractility results.