Pacing-induced congestive heart failure in dogs for 21 days specifically upregulated endothelial NOS protein and Ca2+-dependent NOS activity in the left atria but not ventricles.
Does pacing-induced heart failure alter cardiac NO synthase activity and expression in a chamber-specific manner in dogs?
In a canine model of pacing-induced heart failure, eNOS is specifically upregulated in the left atrium, suggesting a compensatory mechanism against hypertrophy.
In congestive heart failure (CHF) the alterations in cardiac NO synthase (NOS) isoforms activity and expression are incompletely documented and the chamber specificity of these changes is unknown. We studied plasma nitrate-nitrite (NO-x), atrial, and ventricular NOS activities and protein expression (Western blot and densitometric analysis) in nonpaced control dogs and in dogs paced for 2 or 21 days into CHF. Plasma NO-x rose significantly after 7 and 21 days of pacing, whereas creatinine levels remained unchanged. In control dogs Ca2+-dependent NOS activity in left atria was double that of right or left ventricular activity. In paced animals the activity increased only in the atria after 21 but not 2 days of pacing. Levels of endothelial NOS (eNOS) protein were enhanced in the left atria but not ventricles after 21 days of pacing because of a greater quantity of the 150-kDa but not the 135-kDa eNOS. Ca2+-independent NOS activity was undetectable in any cardiac tissue. The specific upregulation of eNOS in the left atria suggests that NO production may be enhanced to counterbalance hypertrophy that develops during pacing-induced CHF.
Khadour et al. (Tue,) conducted a other in Congestive heart failure. Pacing-induced heart failure vs. Nonpaced control dogs was evaluated on Plasma nitrate-nitrite (NO-x), atrial, and ventricular NOS activities and protein expression. Pacing-induced congestive heart failure in dogs for 21 days specifically upregulated endothelial NOS protein and Ca2+-dependent NOS activity in the left atria but not ventricles.