CLINICS 2012;67(5):489-496 Tension cost and contractility changes Moreira CM et al. Figure 2 - Effects of myocardial infarction (A), hypertension (B), diabetes (C), DOCA-salt-induced hypertension (D), and chronic L-NAME treatment (E) on the tetanic peak force (g/mm2) in rat papillary muscle. The results represent the mean ¡ SEM, and N indicates the number of experiments. *p,0.05 vs. control, Sham, NF, Salt, and DOCA (t-test or one-way ANOVA, repeated measurements). reported reductions in force and SERCA2 levels. Hyposensitivity to positive inotropic stimulation with calcium and isoproterenol was also reported (19). These findings are paralleled by the reduction in myosin ATPase activity reported here. Other authors have reported similar findings (27,28), although without the shift of V1 to V3 MHC (28). Wang et al. (9) investigated the time course of myosin ATPase activity after myocardial infarction and found that the level of left ventricular myosin ATPase activity began to decrease at four weeks. These different adaptive changes might result from a phenomenon recently described in rats such that 30-day myocardial infarctions with similar scar areas can behave normally or, alternately, lead to the development of heart failure (25). SHRs develop hypertension and myocardial hypertrophy. These rats have a large period of stable hypertrophy with preserved or enhanced contractile function (23,29). In fact, we did not find differences in force development in these rats compared to WKY rats. Previous reports suggest an increase in contractile force resulting from either increased Ca2+ entry through L-type Ca2+ channels and release from the sarcoplasmic reticulum (29) or enhanced contractility without changes in the levels of contractile proteins but with large calcium spikes (30). However, other reports described reductions in force under steady-state or isoproterenol stimulation (31) resulting from increased calcium uptake by the sarcoplasmic reticulum and an increase in the level of phospholamban phosphorylation. Taken together, these results show that the development of force and the nature of calcium handling change during the evolution of hypertension in SHRs. Our results, however, showed no differences in either the development of force or the level of myosin ATPase activity, suggesting that we studied SHRs with stable contractility function, which explains why the SHRs displayed tension cost similar to that of WKY rats. Regarding the development of tetanic tension, our results demonstrate that under tetanic stimulation, the isometric tension force was not modified in SHRs compared with WKY rats. In accordance with these results, the level of myosin ATPase activity in SHRs was similar to that in WKY rats. Other reports show a reduction in myosin ATPase activity but only after longer periods (32,33). Diabetes is a chronic syndrome resulting from insulin deficiency, which also affects the cardiovascular system. Cardiac contractility dysfunction is described in streptozo- tocin-induced diabetes in rats. Notably, our results are in 493