Abstract
Cardiac functions are modulated by nitric oxide (NO) however the signaling pathways responsible for the cardiac effects of NO are poorly identified. NO regulates cardiac activity through activation of cGMP-dependent protein kinase (PKG) and by alteration of phosphodiesterases (PDEs) activity. This study examined the effects of NO donor diethylamine NONOate (DEA) on the activity of the isolated right atrium and left papillary muscle from the rat heart in the presence of different PDE inhibitors. DEA (0.1–100 μM) decreased contractions and the sinus rate of right atrium but had no effect on the papillary muscle. In the presence of vinpocetine (PDE1 inhibitor) (1–10 μM) or milrinone (PDE3 inhibitor) (1–10 μM), DEA decreased papillary muscle contraction. EHNA (PDE2 inhibitor) (1–10 μM) or sildenafil (PDE5 inhibitor) (1 μM) reversed only DEA-induced decrease in resting force of the right atrium. The effect of DEA on right atrium contractions and the sinus rate was blocked by rolipram (PDE4 inhibitor) (1–10 μM). The present study has indicated that the effect of NO depends on a variety of PDE activities in different regions of the rat heart.
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