ABSTRACT
Introduction:
The intrinsic capacity to aerobic exercise is associated with cardiac inotropism. On the other hand, the contribution of nitric oxide (NO) as an intracellular messenger on Ca2+ dynamics remains unknown in rats with different intrinsic capacities to exercise.
Objective:
To evaluate whether NO modulates differently Ca2+ intracellular transient and spontaneous Ca2+ releases (sparks) in cardiomyocytes of rats with different intrinsic capacities to exercise.
Methods:
Male Wistar rats were selected as standard-performance (SP) and high-performance (HP), according to the exercise capacity until fatigue, assessed through a treadmill progressive stress test. Cardiomyocytes of rats were used to determine Ca2+ intracellular transient and Ca2+ sparks evaluated using confocal microscope. To estimate NO contribution, a NO synthase inhibitor (L-NAME, 100 µM) was used. Data were analyzed through two-way ANOVA followed by Tukey's post hoc test and expressed as means ± SEM.
Results:
Cardiomyocytes of HP rats exhibited higher Ca2+ transient amplitude compared to SP. However, L-NAME increased Ca2+ transient amplitude only in SP rats. No differences were found in Ca2+ transient decay time constant ( t) in cardiomyocytes of SP and HP rats. However, administration of L-NAME caused reduction of tin cardiomyocytes of both groups. Lower amplitude and frequency of Ca2+ sparks were found in cardiomyocytes of HS rats compared to SP group. Administration of L-NAME increased the amplitude of Ca2+ sparks in cardiomyocytes of the HP group.
Conclusion:
NO modulates Ca2+ transient and Ca2+ sparks in cardiomyocytes of rats with different intrinsic exercise capacities.
Keywords:
NG-Nitroarginine methyl ester; physical fitness; myocytes, cardiac; calcium
