Defying the economists: a decrease in heart rate improves not only cardiac but also endothelial function.
Ivabradine has proven therapeutic efficacy for cardiac ischaemia and, until proved otherwise, is a very specific inhibitor of the cardiac sinoatrial node I(f) current. In the current issue of the British Journal of Pharmacology, Drouin et al. demonstrated that chronic treatment of the human apoB-100 transgene dyslipidaemic mouse with ivabradine significantly improved endothelium-dependent vasodilatation to ACh in renal and cerebral arteries and that the beneficial effects of ivabradine result secondarily to the lowering of heart rate. These data suggest that drugs that target the I(f) current have potential benefits not only as anti-ischaemics but also as agents for the treatment of endothelial dysfunction.
Triggle
C R
CR
Department of Pharmacology & Therapeutics, University of Calgary, Calgary, Alberta, Canada. cht2011@qatar-med.cornell.edu
D000818:Animals; D001552:Benzazepines / Q000494:pharmacology* / Q000627:therapeutic use; D002316:Cardiotonic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects*; D006801:Humans; D000077550:Ivabradine; D051379:Mice; D012849:Sinoatrial Node / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects
D001552:Benzazepines; D002316:Cardiotonic Agents; D000077550:Ivabradine