Key result
Cholinergic and purinergic stimulation decreased action potential duration and force of contraction in atrial but not ventricular muscle, and depressed the inotropic response to isoprenaline in both.
Cholinergic and purinergic stimulation depresses beta-adrenergic inotropic responses in both human atrial and ventricular myocardium, but directly affects action potential and contractility primarily in the atria.
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Differential atrial effects may inform selective antiarrhythmic strategies; leaves open clinical translation from isolated human tissue.
The effects of cholinergic and purinergic stimulation on action potential, force of contraction and 86Rb efflux were investigated in human atrial and ventricular heart muscle. 2. In atrial heart muscle, carbachol and (-)-N6-(R-phenyl-isopropyl)-adenosine (R-PIA) and 5'-(N-ethyl)-carboxamido-adenosine (NECA) evoked transient decreases of action potential duration and force of contraction; the steady-state effects on force of contraction were virtually identical to control values. In the presence of propranolol, steady-state values after carbachol, R-PIA or NECA amounted to about 50% of control values. 3. In ventricular heart muscle, carbachol, NECA and R-PIA did not significantly affect the action potential configuration or force of contraction. 4. Carbachol, NECA and R-PIA induced a maintained depression of the positive inotropic response to isoprenaline in both atrial and ventricular heart muscle. 5. The rate constant of 86Rb efflux was slightly increased by carbachol, NECA and R-PIA in atrial (10-20%) but not in ventricular heart muscle. 6. In the presence of isoprenaline, carbachol, NECA and R-PIA did not significantly affect the rate constant of 86Rb efflux in both atrial and ventricular heart muscle. Isoprenaline alone increased the rate constant of 86Rb by about 25% in both tissues.
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Jakob et al. (1989) studied Human isolated atrial and ventricular heart muscle. Cholinergic and purinergic stimulation (carbachol, R-PIA, NECA) vs. Control / isoprenaline alone was evaluated on Action potential, force of contraction, and 86Rb efflux. Cholinergic and purinergic stimulation decreased action potential duration and force of contraction in atrial but not ventricular muscle, and depressed the inotropic response to isoprenaline in both.
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