Extracellular application of the PDE2 inhibitor EHNA increased the amplitude of basal L-type calcium current by approximately 80% in freshly isolated human atrial myocytes.
Does EHNA increase basal L-type Ca2+ current in human atrial myocytes?
Basal L-type calcium current is controlled by PDE2 activity in human atrial myocytes, but not in rat cardiac myocytes, highlighting species-specific regulation of cardiac electrophysiology.
p-value: p=<0.05
-9-2-hydroxy-3-nonyladenine) is a wellknown inhibitor of adenosine deaminase. Recently, EHNA was shown to block the activity of purified soluble cGMPstimulated phosphodiesterase (PDE2) from frog, human, and porcine heart with an apparent K i value of 1 M and with negligible effects on Ca 2 /calmodulin PDE (PDE1), cGMP-inhibited PDE (PDE3), and low K m cAMP-specific PDE (PDE4) (
Rivet-Bastide et al. (Sun,) conducted a other in Patients undergoing heart surgery (n=53). EHNA vs. Basal conditions (control solution) was evaluated on Amplitude of basal L-type Ca2+ current (ICa) (p=<0.05). Extracellular application of the PDE2 inhibitor EHNA increased the amplitude of basal L-type calcium current by approximately 80% in freshly isolated human atrial myocytes.
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