Inotropic effect of harmaline on ventricular and atrial cat myocardium

In isolated cat heart papillary muscle electrically driven, harmaline (HME) concentrations of 4.15 to 16.6 X 10(-5) M induced a dose dependent negative inotropic effect both at temperatures of 30 and 37 C. In fact, HME decreased both peak tension developed (PTD) and velocity of development of tension (dT/dt) and increased time to peak tension (TPT). The same concentrations induced also a dose-dependent increase of the effective refractory period (ERP). Concentrations of HME lower than 4.15 X 10(-5) M did not show any effect in papillary muscle. In isolated atria of the same cats either spontaneously beating or electrically driven, at 30 C, HME induced a dual inotropic effect. In fact, concentrations of 8.3 X 10(-5) M and 24.9 X 10(-5) M induced an increase in both PTD and dT/dt and lengthening of time to peak tension (TPT). Higher HME concentrations such as 41.5 X 10(-5) M induced a decrease in dT/dt, a negative inotropic effect, but still lengthened the TPT. In both preparations, whenever the dT/dt was depressed the PTD was diminished in spite of the prolongation of TPT. The lesser density of adrenergic innervation and catecholamines concentration in papillary muscle than in atrial myocardium probably explains the negative inotropic action of HME in ventricular myocardium as compared to the dual inotropic effect observed in atria.