ArticleBritish journal of pharmacology2007
Is there a functional correlate of Kv1.5 in the ventricle of canine heart and what would it mean for the use of I(Kur) blockers?
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart.Journal of diabetes research · 2018Article
- Polyunsaturated Fatty acids modify the gating of kv channels.Frontiers in pharmacology · 2012Article
- Safety of the novel atrial-selective K+-channel blocker AVE0118 in experimental heart failure.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
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Abstract
The cardiac ultrarapid outward current I(Kur), encoded by KCNA5, is of special pharmacological interest, because it is considered to be atrium-specific. I(Kur) has therefore become a target in the therapy of atrial tachyarrhythmias. However, the concept of atrium specificity is only valid if a functional I(Kur) current is in fact absent from the ventricle. However, new work has detected a I(Kur)-like current in canine ventricular myocytes, sensitive to 4-aminopyridine and suppressed by the I(Kur) blocker DPO-1, findings that support the existence of a functional ventricular I(Kur). These indications are, however, indirect and more effort is needed to clarify unequivocally the putative role of an expectedly small I(Kur) component in the ventricle.
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