Previous studies demonstrated that transition from compensatory pressure overload hypertrophy to decompensatory volume overload heart failure is associated with decreased cardiac tensile strength and activation of matrix metalloproteinase (MMP) in spontaneously hypertensive rat (SHR). To test the hypothesis that in the absence of nitric oxide activation of MMP during cardiac failure causes disruption in the organization of extracellular matrix (ECM) and leads to decrease systolic and diastolic cardiac tensile strength, we employed SHR of 24--32 weeks, which demonstrates significant cardiac hypertrophy and fibrosis. The normotensive Wistar rats (NWR) were used as control. To determine whether cardiac hypertrophy is associated with increased elastinolytic matrix metalloproteinase-2 (MMP-2) activity; quantitative elastin-zymography was performed on cardiac tissue homogenates. The MMP-2 activity was normalized by the levels of actin. The MMP-2/actin ratio was 2.0+/-0.5 in left ventricle (LV) and 1.5+/-0.25 in right ventricle (RV) of SHR(32wks); and 0.5+/-0.25 in LV and 0.25+/-0.12 in RV of NWR(32wks) (P<0.02 when SHR compared with NWR). To measure passive diastolic cardiac function, rings from LV as well as RV through transmyocardial wall from male SHR and NWR of 6--8 weeks and 24--36 weeks were prepared. The LV wall thickness from endocardium to epicardium was 3.75+/-0.25 mm in SHR(32wks) as compared to 2.25+/-0.50 mm in NWR(32wks) (P<0.01). The ring was placed in tissue myobath and length--tension relationships were assessed. The pressure--length relationship was shifted to left in SHR as compared to NWR. The amounts of cardiac elastin and collagen were determined spectrophotometrically by measuring desmosine--isodesmosine and hydroxyproline contents, respectively. A negative correlation between elastic tensile strength and elastin/collagen ratio was elucidated. To create situation analogous to heart failure and MMP activation, we treated cardiac rings with active MMP-2 and length--tension relation was measured. The relationship was shifted to right in both SHR and NWR when compared to their respective untreated groups. The results suggested that activation of MMP led to decreased cardiac tissue tensile strength and may cause systolic and diastolic dysfunction.