| Popis: |
The sarcoplasmic reticulum (SR) exerts a key role on the excitation-contraction coupling process in the myocardium. Since the relation between the volume of cellular organelles, such as SR, and the sarcolemmal area of myocytes is not uniform in myocardial hypertrophy of different etiologies, we compared the contractile performances of hypertrophied left ventricular papillary muscles from rats with pressure overload and with volume overload. Hemodynamically compensated spontaneous hypertensive rats (SHR, 3 months old, systolic blood pressure = 189 +/- 4 mmHg, n = 8) and Wistar rats with healed (30 days) myocardial infarction (MI, n = 7) produced by ligation of the left coronary artery were used. Results were compared with age-matched Wistar control (CON) rats (n = 13). Force (F), corrected to muscle cross-sectional area (g/mm2), and dF/dt were recorded in muscles contracting isometrically and stretched to Lmax. The inotropic response to increasing extracellular Ca2+ concentrations (1.25 to 5.0 mM) was compared in twitches (0.5 Hz) and during tetanic stimulation (5 Hz, 30 s) in the muscles treated with 1 microM ryanodine. F recorded in basal conditions (Ca = 1.25 mM, 0.5 Hz) in the CON group (1.34 +/- 0.20 g/mm2) was higher (p0.05) than in the MI (0.73 +/- 0.13 g/mm2) and lower (p0.05) than in the SHR group (2.08 +/- 0.25 g/mm2). Similar differences between groups were also observed in relation to +dF/dt. Increasing extracellular Ca produced a parallel increase of F and +dF/dt in the three groups of muscles. Ryanodine treatment reduced F and +dF/dt in all groups and completely inhibited the development of force in post-rest contractions, indicating SR inhibition. SHR muscles were more sensitive to ryanodine than CON and MI (F decrease = 64 +/- 7, 51 +/- 5, and 22 +/- 5%, respectively, p0.05). The tetanic tension (Ca = 1.25 mM) was similar in SHR and CON (0.82 +/- 0.19 and 0.92 +/- 0.18 g/mm2; p0.05) and depressed in the MI group (0.35 +/- 0.12 g/mm2). These data suggest an increased participation of SR as source of activator Ca in the hypertrophied muscle of SHR. This adaptation likely contributes to maintain the normal cardiac function in hemodynamically compensated SHR, despite increasing afterload levels. This adaptation seems not to occur after MI, which may contribute to the depressed contractile performance of the left ventricular muscle surviving to infarction. |
