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Effect of long-term treatment with beta-blocker on cardiac hypertrophy in SHR
Insights
Beta-blocker therapy attenuated cardiac hypertrophy and myocardial degeneration in spontaneously hypertensive rats. However, this treatment did not alter the transition of cardiac myosin isozymes during overload adaptation.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Cardiac hypertrophy is a common response to pressure overload.
- Beta-blocker treatment is suggested to attenuate cardiac hypertrophy.
- The effect of beta-blockers on intracellular cardiac constituents during hypertrophy is not well understood.
Purpose of the Study:
- To investigate the impact of chronic beta-blocker administration on cardiac myosin isozymes and histology in spontaneously hypertensive rats.
- To assess the effects of carteolol and propranolol on cardiac hypertrophy and intracellular changes.
Main Methods:
- Spontaneously hypertensive rats were treated with carteolol or propranolol for 4, 12, or 30 weeks.
- Cardiac myosin isozyme composition, histological findings, and heart weight were analyzed.
- Blood pressure was monitored throughout the study.
Main Results:
- Beta-blocker treatment suppressed cardiac hypertrophy, evidenced by reduced left ventricular weight, without significantly lowering blood pressure.
- Myocardial degeneration and reactive fibrosis were alleviated by 12 weeks of beta-blocker treatment.
- The transition of cardiac myosin isozymes (V1 to V2/V3) remained unaffected by beta-blocker therapy.
Conclusions:
- Chronic beta-blocker administration attenuates cardiac hypertrophy and myocardial degeneration in spontaneously hypertensive rats.
- Beta-blockers do not influence the transition of cardiac myosin isozymes, a biochemical adaptation to myocardial overload.
- These findings suggest beta-blockers mitigate structural damage without altering specific biochemical adaptive responses in the hypertrophied heart.
Abstract:
Recent studies suggest that beta-blocker treatment may attenuate cardiac hypertrophy induced by pressure overload in the spontaneously hypertensive rat (SHR), but the effect of this therapy on the reconstitution of the intracellular constituents in the heart that occurs during the development of cardiac hypertrophy has not been examined. In this study, we investigated the effect of chronic administration of carteolol (4 mg/kg/day p.o.) or propranolol (20 mg/kg/day p.o.), beta-blockers with distinct modes of action, on the composition of cardiac myosin isozymes and histological findings as well as heart weight. Therapeutic periods were 4, 12 or 30 weeks. Though blood pressure was not significantly reduced, the development of cardiac hypertrophy was suppressed as evidenced by left ventricular weight in both groups of carteolol- and propranolol-treated SHR for all therapeutic periods. Again, beta-blocker treatment for 12 weeks alleviated myocardial degeneration and reactive fibrosis which were observed in all cases of age-matched untreated SHR. However the extent of the transition of cardiac myosin isozymes from V1 to V2 or V3 were essentially the same among all groups including untreated SHR. These results indicate that chronic administration of beta-blockers attenuates the development of cardiac hypertrophy and degeneration without affecting the transition of myosin isozymes which is thought to be a kind of biochemical adaptation of the myocardium to overload.