In isolated dog atria, dopamine alters sinoatrial conduction time via beta-adrenergic mechanisms and tyramine-like action, with the direction of effect dependent on baseline sinus cycle length.
Answers are grounded in this paper and cite their sources.
These isolated canine findings should not guide clinical dopamine use; leaves open human sinus node effects.
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.
No takes yet. Share an insight, caveat, or question.
Kobayashi et al. (1984) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: