COMPARISON OF THE CONTRACTILE PERFORMANCE OF THE HYPERTROPHIED MYOCARDIUM FROM SPONTANEOUS HYPERTENSIVE RATS AND NORMOTENSIVE INFARCTED RATS

The sarcoplasmic reticulum (SR) exerts a key role on the excitation-co ntraction coupling process in the myocardium. Since the relation betwe en 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 a nd with volume overload. Hemodynamically compensated spontaneous hyper tensive rats (SHR, 3 months old, systolic blood pressure = 189 +/- 4 m mHg, n = 8) and Wister rats with healed (30 days) myocardial infarctio n (MI, n = 7) produced by ligation of the left coronary artery were us ed. Results were compared with age-matched Wistar control (CON) rats ( n = 13). Force (F), corrected to muscle cross-sectional area (g/mm(2)) , and dF/dt were recorded in muscles contracting isometrically and str etched to L-max. The inotropic response to increasing extracellular Ca 2+ concentrations (1.25 to 5.0 mM) was compared in twitches (0.5 Hz) a nd during tetanic stimulation (5 Hz, 30 s) in the muscles treated with 1 mu M ryanodine. F recorded in basal conditions (Ca = 1.25 mM, 0.5 H z) in the CON group (1.34 +/- 0.20 g/mm(2)) was higher (p < 0.05) than in the MI (0.73 +/- 0.13 g/mm(2)) and lower (p < 0.05) than in the SH R group (2.08 +/- 0.25 g/mm(2)). Similar differences between groups we re also observed in relation to +dF/dt. Increasing extracellular Ca pr oduced a parallel increase of F and +dF/dt in the three groups of musc les. Ryanodine treatment reduced F and +dF/dt in all groups and comple tely inhibited the development of force in post-rest contractions, ind icating SR inhibition. SHR muscles were more sensitive to ryanodine th an CON and MI (F decrease = 64 +/- 7, 51 +/- 5, and 22 +/- 5%, respect ively, p < 0.05). The tetanic tension (Ca = 1.25 mM) was similar in SH R and CON (0.82 +/- 0.19 and 0.92 +/- 0.18 g/mm(2); p > 0.05) and depr essed in the MI group (0.35 +/- 0.12 g/mm2). These data suggest an inc reased participation of SR as source of activator Ca in the hypertroph ied muscle of SHR. This adaptation likely contributes to maintain the normal cardiac function in hemodynamically compensated SHR, despite in creasing 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.