Journal
GENERAL PHYSIOLOGY AND BIOPHYSICS
Volume 37, Issue 2, Pages 153-162Publisher
GENERAL PHYSIOL AND BIOPHYSICS
DOI: 10.4149/gpb_2017025
Keywords
Hypertrophy/heart failure; Monocrotaline; Renin-angiotensin-aldosterone system; Angiotensin II type-1 (AT(1)) receptors; Slow force response; Ca2+ transient
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Funding
- Russian Foundation for Basic Research [16-04-00545]
- Program for Basic Research of Ural Branch of the Russian Academy of Sciences [15-5-4-6]
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The slow force response (SFR) of a cardiac muscle to a sudden stretch is thought to be important in the regulatory adaptation of myocardial contraction. Autocrine-paracrine regulation pathways which involve angiotensin II are participating in this mechanism. On the other hand, renin-angiotensin-aldosterone system (RAS) is altered in hypertrophic or failing myocardium. We compared the effects of sudden stretch to SFR as well as to twitch and Ca2+ transient characteristics in rat myocardium with monocrotaline-induced heart failure with those in normal rat myocardium without and with inhibition of angiotensin II type-1 (AT(1)) receptors. Our findings indicate that the myocardium of rats with monocrotaline-induced right ventricular failure is deficient with activation of local RAS and therefore expresses blunted SFR, very similar to the depression of SFR observed in normal myocardium under inhibition of AT(1) receptors. The failing myocardium does not further respond to the putative inhibition of AT(1) receptors by losartan. In conclusion, SFR is related to autocrine-paracrine regulation of myocardial contraction in normal rat myocardium and that the involvement of RAS into stretch-induced modulation of contractility may be significantly altered in failing heart.
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