Increases in internal dimensions of the chambers of the heart (cardiac dilatation), mediated by right shifts in cardiac chamber diastolic pressure-volume (P-V) relations, predict mortality in patients with established heart failure. However, the mechanisms responsible for the transition from concentric cardiac hypertrophy to cardiac dilatation are unclear. Recent evidence suggests that decreases in the cross-linked properties of myocardial collagen may increase the propensity of collagen to cleavage and hence reduce cardiac myocyte tethering, thus promoting cardiac dilatation. However, decreases in myocardial collagen cross-linking may also reduce myocardial stiffness, thus explaining right shifts in cardiac diastolic P-V relations. In the present dissertation I evaluated whether right shifts in diastolic P-V relations produced by chronic β-adrenoreceptor activation (isoproterenol, a β-adrenoreceptor agonist, 0.02 mg.kg-1.day) in spontaneously hypertensive rats (SHR) with compensated cardiac hypertrophy (12 months of age), can be explained by adverse chamber remodelling or alterations in the myocardial material properties of the heart. After 7 months of daily isoproterenol administration, SHR had marked right shifts in left ventricular (LV) diastolic P-V relations as determined in isolated, perfused hearts, with increases in the volume intercept of these relations, a change that translated into increases in LV cavity diameters (echocardiography). LV dilatation was associated with reductions in LV pump function (decreases in LV endocardial fractional shortening and the slope of the LV systolic P-V relation [LV E]). The reductions in pump function were attributed to the LV dilatation rather than to alterations in intrinsic myocardial contractile properties as LV midwall fractional shortening and myocardial systolic elastance (LV En) were unchanged. Although SHR not receiving isoproterenol had increases in the LV diastolic wall thickness-to-radius ratio, a change commensurate with compensatory concentric LV hypertrophy, LV wall thickness-to-radius ratio in SHR exposed to chronic β-adrenoreceptor activation was reduced to values similar to those noted in normotensive Wistar Kyoto (WKY) control rats, despite further increases in LV weight. SHR not receiving isoproterenol had a marked increase in myocardial stiffness (slope of the linearized LV diastolic stress-strain relationship) as compared to WKY rats, a change that was associated with an increased myocardial collagen of the cross-linked phenotype. Although SHR receiving daily isoproterenol had further increases in myocardial collagen, this did not translate into changes in LV diastolic myocardial stiffness, as the further increase in myocardial collagen was of the non cross-linked phenotype. However, through a susceptibility to digestion, this collagen phenotype could have contributed to LV dilatation. In conclusion, these data suggest that LV dilatation in SHR following chronic β-adrenoreceptor activation is attributed to adverse chamber remodelling rather than to alterations in myocardial material properties as indexed by diastolic stress-strain relations.