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FOR AUTHORS General Physiology and Biophysics 2018 General Physiology and Biophysics Vol.37, No.2, p.153–162, 2018
FOR AUTHORS General Physiology and Biophysics 2018 General Physiology and Biophysics Vol.37, No.2, p.153–162, 2018
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General Physiology and Biophysics Vol.37, No.2, p.153–162, 2018 |
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| Title: Inhibition of AT1 receptors by losartan affects myocardial slow force response in healthy but not in monocrotaline-treated young rats | ||
| Author: Oleg Lookin, Alexandr Balakin, Yuri Protsenko | ||
| Abstract: 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 (AT1) 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 AT1 receptors. The “failing” myocardium does not further respond to the “putative” inhibition of AT1 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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| Keywords: Hypertrophy/heart failure — Monocrotaline — Renin-angiotensin-aldosterone system — Angiotensin II type-1 (AT1) receptors — Slow force response — Ca2+ transient | ||
| Published online: 27-Mar-2018 | ||
| Year: 2018, Volume: 37, Issue: 2 | Page From: 153, Page To: 162 | |
| doi:10.4149/gpb_2017025 |
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