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The hypothalamic nonapeptides oxytocin and arginine vasopressin promote cardiac myocyte survival in rats with heart failure
Author(s) -
Salikova Svetlana P,
Stadnikov Alexander A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1130.3
Subject(s) - vasopressin , oxytocin , medicine , endocrinology , hypothalamus , heart failure , phenylephrine , supraoptic nucleus , arginine , myocyte , chemistry , blood pressure , biochemistry , amino acid
The current study examines the hypothesis that the hypothalamic nonapeptides oxytocin (OT) and arginine vasopressin (AVP) are involved in morphogenic modulation of LV remodeling during development of heart failure in rats. Experimental heart failure (HF) has been induced in male Wistar rats (180–230g) by i.m. injections of 0.1 ml 1% mesatonum (phenylephrine) solution and subsequent swimming until exhaustion for 10 days. The small pieces of LV myocardium from the hearts of control and HF rats were explanted for 3 days in medium 199 supplemented with 20 % FBS. The explants were treated with OT (0.5·10 −5 IU) or AVP (0.5·10 −5 IU) for 72 hrs. The LV myocardium and the hypothalamic‐hypophyseal neurosecretory system (HHNS) were analyzed using light and electron microscopy. The presence of apoptotic cells were detected using TUNEL technique and p53 immunohistochemistry. We found that OT and AVP similarly reduced the number of necrotic and apoptotic cardiac myocytes compared to untreated explants (~4% and ~2% vs. ~15% and ~10%, respectively, P<0.05). However, although neurosecretory cells of the paraventricular and supraoptic nuclei of the hypothalamus were activated in rats with HF, there were signs of inhibition of release of OT and AVP from neurohypophysial terminals. Thus, we suggest that OT and AVP demonstrate a cardioprotective potential by preventing the cardiac myocyte death and that the inhibition of their release from the HHNS during development of heart failure might play a modulatory role in progression of LV remodeling.