Open AccessInhibition of AT1 receptors by losartan affects myocardial slow force response in healthy but not in monocrotaline-treated young rats
Author(s) -
Oleg Lookin,
Alexandr Balakin,
Yuri Protsenko
Publication year - 2018
Publication title -
general physiology and biophysics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.376
H-Index - 39
eISSN - 1338-4325
pISSN - 0231-5882
DOI - 10.4149/gpb_2017025
Subject(s) - losartan , angiotensin ii receptor type 1 , paracrine signalling , medicine , autocrine signalling , contractility , angiotensin ii , endocrinology , receptor , heart failure , contraction (grammar) , renin–angiotensin system , angiotensin receptor , cardiology , blood pressure
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.