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PubMed2000

Chronic AT(1) blockade stimulates extracellular collagen type I degradation and reverses myocardial fibrosis in spontaneously hypertensive rats.

It has been suggested that left ventricular fibrosis in spontaneously hypertensive rats (SHR) is the result of both exaggerated collagen synthesis and insufficient collagen degradation. We have shown previously that chronic treatment with the angiotensin II type 1 receptor antagonist losartan results in diminished synthesis of collagen type I molecules and reversal of myocardial fibrosis in SHR. This study was designed to investigate whether losartan also affects the extracellular degradation of collagen type I fibers in the left ventricle of SHR. The study was performed in 30-week-old normotensive Wistar-Kyoto rats (WKY), untreated SHR, and SHR treated with orally administered losartan (20 mg/kg per day) for 14 weeks before they were killed. Ventricular collagenase activity was determined by degradation of [(14)C]collagen with tissue extracts. Ventricular expression of tissue inhibitor of metalloproteinases 1 (TIMP-1) mRNA was analyzed by Northern blot. A histomorphometric study of the left ventricle was performed in all rats. Compared with WKY, SHR exhibited left ventricular hypertrophy, increased (P<0.05) blood pressure, left ventricular collagen volume fraction and TIMP-1 mRNA, and diminished (P<0.05) collagenase activity. After the treatment period, blood pressure was higher (P<0.05) in losartan-treated SHR than in WKY, and no significant differences were noted in the remaining parameters between the 2 strains of rats. Compared with untreated SHR, treated SHR showed no left ventricular hypertrophy, diminished (P<0.05) blood pressure, left ventricular collagen volume fraction and TIMP-1 mRNA, and increased (P<0.05) collagenase activity. These results suggest that the transcription of the TIMP-1 gene is upregulated in the hypertrophied and fibrotic left ventricle of adult SHR. Upregulation of TIMP-1 may account for diminished collagenase activity in the myocardium of those rats. Chronic angiotensin II type 1 receptor blockade with losartan resulted in inhibition of TIMP-1 expression and stimulation of collagenase activity in the left ventricle of SHR. It is proposed that angiotensin II may facilitate myocardial fibrosis in SHR by depressing the collagenase-mediated extracellular degradation of collagen fibers.

Angiotensin Receptor Antagonists↗
PubMed1986

Release of unassembled rat cardiac myosin light chain 1 following the calcium paradox.

To determine the intracellular source and release kinetics of myosin light chain 1 immediately following irreversible myocytic injury, we perfused rat hearts in a Langendorff apparatus under control conditions (20 minutes), or during global cellular injury produced by oxygenated, calcium-free perfusion (5 minutes), followed by reperfusion with buffer containing 2.5 mM calcium (15 minutes). Light chain 1 concentration (double antibody radioimmunoassay) and creatine kinase activity were measured in both the coronary effluent and the 140,000 g supernatant extract of perfused ventricular tissue (after homogenization and ultracentrifugation). Calcium reperfusion caused the rapid release of both light chain 1 and creatine kinase activity (peak light chain 1 = 1.09 +/- 0.19 micrograms/g; peak creatine kinase = 74.9 +/- 10.7 IU/ g at 1 minute, mean +/- SD, n = 3); 28.5 +/- 13.5% of total light chain 1 and 86.5 +/- 0.6% of total creatine kinase activity were depleted from the tissue extract during the 15-minute reperfusion. No light chain 1 or creatine kinase was detected in the effluents of control-perfused hearts. Dodecyl sulfate polyacrylamide gel electrophoresis and immunodetection with specific antibody to myosin heavy chain and light chain 1 showed that the effluent light chain 1 was of similar molecular weight (mol wt = 27,000) to the subunit bound to myofibrils. In addition, light chain 1 was released in the absence of myosin heavy chain. Thus, a small soluble pool of unassembled myosin light chain 1 subunits exists in the cytoplasm of cardiac myocytes that is released from irreversibly injured cells. This pool demonstrates initial washout kinetics similar to creatine kinase.

Animals↗