2024/08/05 by U. Gergs, Ulrich Gergs, T. H. Pham +13
Medicine · #Cardiac Arrhythmias and Treatments #Cardiac electrophysiology and arrhythmias #Cardiac pacing and defibrillation studies
paper · pdf · doi:10.1007/s00210-024-03340-z
crossref issued 2024/08/05 · crossref published 2024/08/05 · crossref published-online 2024/08/05 · openalex publication_date 2024/08/05 · crossref created 2024/08/05 · openalex created_date 2024/08/06 · crossref published-print 2025/02/01 · crossref deposited 2025/02/13 · crossref indexed 2026/07/30 · openalex updated_date 2026/07/31
Abstract Dopamine receptors have been claimed not to directly increase contractility in the human heart. Therefore, we performed contraction experiments in isolated electrically driven human atrial preparations (HAP). For comparison, we performed contraction experiments with left atrial preparations of transgenic mice which harbor a cardiac overexpression of human D 1 -dopamine receptors (D 1 -TG). In D 1 -TG, first we noted that dopamine (10 nM–10 µM cumulatively applied) in the presence of propranolol exerted a concentration- and time-dependent positive inotropic effect in D 1 -TG. In a similar fashion, dopamine increased force of contraction in the presence of 0.4 µM propranolol in HAP and these effects were amplified by pre-treatment with inhibitor of phosphodiesterase III (1 µM) cilostamide. Moreover, contractile effects of dopamine in the presence of propranolol 0.4 µM in HAP were antagonized by odapipam, haloperidol, or raclopride. Ten micromolars of fenoldopam in the presence of cilostamide increased force of contraction in HAP and this effect was antagonized by SCH 23390. We conclude that stimulation of human D 1 -dopamine receptors can increase force of contraction in the HAP.