Effects of dopamine on sinoatrial conduction in isolated, blood-perfused dog atria.

Abstract

Dopamine, administered at a constant infusion rate of 1-2 micrograms/min into the cannulated sinus node artery of the isolated dog atrium, decreased sinus cycle length (SCL) from 630 +/- 19 to 501 +/- 22 msec (mean +/- SEM, 38 trials in 12 atria). However, on sinoatrial conduction time (SACT) estimated by a constant atrial pacing method, dopamine produced 2 types of response (shortening and lengthening) with sinus tachycardia. In 24 trials in 11 atria, the drug decreased SACT from 86 +/- 8 to 56 +/- 4 msec, and in 14 trials in 6 atria it increased SACT from 67 +/- 7 to 101 +/- 9 msec. In general, the effects of dopamine on SACT were dependent on the control levels of SCL: dopamine caused a reduction of SACT at small levels of SCL and a prolongation at large levels. At a control sinus rate of 120 beats/min, dopamine usually shortened SACT. Dopamine-induced shortening of SACT was blocked by a beta-adrenoceptor blocker, propranolol, and an uptake blocker, imipramine, but not by a dopaminergic inhibitor, sulpiride. Furthermore, dopamine-induced lengthening of SACT tended to be suppressed by propranolol, but not by sulpiride. It is concluded that the dopamine-induced changes in SACT are mediated via beta-adrenergic mechanism and partially due to a tyramine-like action.