The present study was designed to investigate the effect of
5-aminoisoquinoline, a specific
poly(ADP-ribose) polymerase (
PARP) inhibitor, in partial abdominal aortic constriction (PAAC) for 4 weeks it induced pathological and chronic swimming training (CST) for 8 weeks it induced physiological
cardiac hypertrophy.
5-Aminoisoquinoline (0.3 mg/kg/day and 3 mg/kg/day, i.p.) treatment was started 3 days before PAAC and CST, and it was continued for 4 weeks after PAAC and 8 weeks after initiation of CST. The left ventricular (LV) function and LV
hypertrophy were assessed by measuring LVDP, dp/dtmax, dp/dtmin, ratio of LV weight to
body weight (LVW/BW), LV wall thickness (LVWT), LV
collagen content, LV
protein content, and LV
RNA concentration. Further, venous pressure (VP) and mean arterial blood pressure (MABP) were recorded. The PAAC, but not CST, produced
LV dysfunction by decreasing LVDP, dp/dtmax, dp/dtmin, and increasing LV
collagen content. Further, PAAC and CST were noted to produce LV
hypertrophy by increasing LVW/BW, LVWT, LV
protein content, and LV
RNA concentration. Moreover, in contrast to CST, PAAC significantly increased VP and MABP. The
5-aminoisoquinoline, a potent selective inhibitor of PARP, significantly attenuated PAAC-induced
LV dysfunction, LV
hypertrophy, increase in VP and MABP. On the other hand, treatment with
5-aminoisoquinoline did not modulate CST-induced physiological
cardiac hypertrophy. These results implicate PARP in PAAC-induced
LV dysfunction and pathological
cardiac hypertrophy. However, PARP may not be involved in CST-induced physiological
cardiac hypertrophy.