Glucose-dependent insulinotropic polypeptide exhibited positive inotropic effects on the human atrium.
Does glucose-dependent insulinotropic polypeptide (GIP) improve force of contraction in isolated human and mouse atrial preparations?
Functional GIP receptors are present in human and mouse atria and mediate positive inotropic effects.
Glucose-dependent insulinotropic polypeptide formerly called gastrin inhibitory peptide (GIP), a peptide composed of 42 amino acids, is formed in duodenal and jejunal cells. GIP acts via GIP receptors (GIPR). GIPR can stimulate adenylyl cyclases (AC) and increase intracellular cyclic adenosine-3´,5´-monophosphate (cAMP) levels. The physiological role of GIPR in the human heart is not fully understood. Thence, force of contraction (FOC) was studied in isolated electrically driven (1 Hz) human right atrial preparations from patients undergoing bypass surgery due to severe coronary heart disease. We noted that in paced human atrium, GIP increased FOC. This effect was reduced by a GIPR-antagonist (ProGIP). In the presence of 0.1 µM cilostamide, a phosphodiesterase (PDE) 3 inhibitor, the positive inotropic effects (PIE) of GIP were more potent and efficient to raise FOC. Up to 100 nM GIP failed to heighten the spontaneous beating rate in mouse right atrial preparations, but increased FOC in electrically driven left atrial mouse preparations but only in the presence of a PDE 4 inhibitor (100 nM rolipram). We conclude that the human atrium and the mouse atrium contain functional GIPR with respect to FOC.
Neumann et al. (Wed,) conducted a other in Human atrial function. glucose-dependent insulinotropic polypeptide vs. null was evaluated on Positive inotropic effects as assessed in the human atrium. Glucose-dependent insulinotropic polypeptide exhibited positive inotropic effects on the human atrium.