Effect of glucagon on the transmembrane potential, contraction, and ATPase activity of the failing human heart

The effects of glucagon (5, 10, 20, and 50 μg/ml.) on the simultaneously recorded transmembrane potentials and contractions; and (Na+—K+)-ATPase activity of 24 papillary muscles obtained from 24 patients undergoing corrective open heart surgery were investigated. Glucagon in all the concentrations produced an increase in the force of contraction associated with a shortening of the action potential duration in two papillary muscles obtained from patients suffering from mild heart failure. The maximal percent increases in contraction produced by 5, 10, 20, and 50 (μg/ml. glucagon were 15 ± 4 (SD), 25 ± 3·5, 42 ± 4, and 44 ± 4 respectively. Glucagon did not produce any significant change in the transmembrane potential in 18 papillary muscles obtained from patients suffering from chronic heart failure. (Na+—K+)-ATPase activity of human papillary muscle was found to be 21·53 ± 1·37 (SE) μ-mole/mg protein/hr. Glucagon in none of the concentrations produced any significant change in the Na+—K+-ATPase activity. These results indicated that glucagon might not be effective in the chronic heart failure because it did not increase the contractility in such muscles. Also glucagon induced positive inotropic effect seems to be associated with a shortening of the action potential duration.