Mechanisms underlying the genesis of post-extrasystolic potentiation in rat cardiac muscle
Vassallo, D.V.; Lima, E.Q.; Campagnaro, P.; Faria, A.N.; Mill, J.G.
Brazilian Journal of Medical and Biological Research 28(3): 377-383
1995
ISSN/ISBN: 0100-879X PMID: 8520535 Document Number: 447033
Changes of contractility resulting from changes in stimulation pattern (post-extrasystolic potentiation - PESP) were investigated in right ventricular papillary muscles from female albino rats (EPM strain, 160-200 g). The preparations were superfused with bicarbonate buffered solution at 24 +- 0.5 degree C, and stimulated at 0.5 Hz. Maintained paired stimulation was performed at several coupling intervals (360, 500, 660, 770 and 920 ms) with normal Krebs for 30 s. After treatment with ryanodine (1 mu-M), used as an inhibitor of the release. of sarcoplasmic reticulum Ca-2+ activity, the same protocol was repeated in the presence of normal Krebs, low Na+ (80 mM, LiCl used as substitute) and low K+ concentrations to change the level of activity of the Na+/Ca-2+ exchange mechanism. With normal Krebs, paired pulse stimulation produced a maintained potentiation of the post-extrasystolic beat and an extrasystole with a reduced force generation when compared to the control steady-state contraction. As the interval between the extrasystole and the normal beat was increased the potentiation of the post-extrasystolic beat was reduced and the force of the extrasystole was increased. Ryanodine treatment reduced the force of contraction and increased its duration, and the pattern of the PESP phenomenon was altered. Both the post-extrasystolic and the extrasystolic beats were potentiated compared to the steady-state contraction obtained under ryanodine treatment. The extra-systole displayed a greater potentiation than the post-extrasystolic beat. As the interval between them increased the amplitude of the extrasystolic beat was enhanced. The differences in peak force between the extrasystolic and the post-extrasystolic beats were almost abolished during the treatment with ryanodine and at low extracellular Na+ concentration. This maneuver decreases the intracellular Na+ enhancing Ca-2+ extrusion by the Na+/Ca-2+ exchanger. The resulting intracellular Ca-2+ reduction decreases peak force and the differences between the extrasystolic and the post-extrasystolic beats. The low K+ concentration enhanced the pattern displayed after ryanodine treatment at normal K+ concentration. It may be concluded that the characteristics of the potentiation phenomenon promoted by the paired stimulation under control conditions depend on the activities of the sarcoplasmic reticulum and of the Na+/Ca-2+ exchange mechanism.