L-NAME treatment enhances exercise-induced content of myocardial heat shock protein 72 (Hsp72) in rats.

BACKGROUND/AIM: Nitric oxide (NO) modulates the expression of the chaperone Hsp72 in the heart, and exercise stimulates both NO production and myocardial Hsp72 expression. The main purpose of the study was to investigate whether NO interferes with an exercise-induced myocardial Hsp72 expression.

METHODS

Male Wistar rats (70-100 days) were divided into control (C, n=12), L-NAME-treated (L, n=12), exercise (E, n=13) and exercise plus L-NAME-treated (EL, n=20) groups. L-NAME was given in drinking water (700 mg·L(-1)) and the exercise was performed on a treadmill (15-25 m·min(-1), 40-60 min.day(-1)) for seven days. Left ventricle (LV) protein Hsp content, NOS and phosphorylated-NOS (p-NOS) isoforms were measured using Western blotting. The activity of NOS was assayed in LV homogenates by the conversion of [(3)H]L-arginine to [(3)H]L-citrulline.

RESULTS

Hsp72 content was increased significantly (223%; p < 0.05) in the E group compared to the C group, but exercise alone did not alter the NOS content, p-NOS isoforms or NOS activity. Contrary to our expectation, L-NAME enhanced (p < 0.05) the exercise-induced Hsp72 content (EL vs. C, L and E groups = 1019%, 548% and 457%, respectively). Although the EL group had increased stimulatory p-eNOS(Ser1177) (over 200%) and decreased inhibitory p-nNOS(Ser852) (ñ50%) compared to both the E and L groups (p < 0.05), NOS activity was similar in all groups.

CONCLUSIONS

Our results suggest that exercise-induced cardiac Hsp72 expression does not depend on NO. Conversely, the in vivo L-NAME treatment enhances exercise-induced Hsp72 production. This effect may be due to an increase in cardiac stress.