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Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Author:
De Gobbi, Juliana Irani Fratucci, Omoto, Ana Carolina Mieko, Siqueira, Tamires Ferreira, Matsubara, Luiz Shigueto, Roscani, Meliza Goi, Matsubara, Beatriz Bojikian
Source:
Physiology & behavior 2015 v.144 pp. 124-128
ISSN:
0031-9384
Subject:
antidepressants, cardiac output, echocardiography, excretion, heart, heart failure, heart valve diseases, hypertrophy, males, patients, photosynthetically active radiation, prognosis, rats, serotonin, sodium chloride, surgery
Abstract:
Depression is a predictor of poor prognosis in patients with heart failure. Selective serotonin (5-HT) reuptake inhibitors (SSRIs) may improve these outcomes. Left ventricular volume overload induced hypertrophy that is associated with aortic regurgitation (AR) leads to ventricular dysfunction and heart failure. The aim of this study was to verify the effects of the SSRI paroxetine on cardiac function, as well as on fluid intake and excretion, in subchronic AR. Male Wistar rats (260 to 280g) received sham (SH) surgery or AR induced by retrograde puncture of the aortic valve leaflets. The presence of AR was confirmed by echocardiography (ECHO) exams. Four weeks after AR surgery, subcutaneous injections of paroxetine (PAR: 10mg/kg 3 times in a week) or saline were administered. The rats were randomly divided into the following 4 groups and treated for 4 weeks: AR-PAR, ARsaline, SH-PAR and SH-saline. At the end of the treatment period, fractional shortening was preserved in AR-PAR, compared to AR-saline (46.6±2.7% vs 38.3±2.2%, respectively). Daily 0.3 M NaCl intake was reduced in PAR-treated rats. Natriuresis was increased in weeks 2-3 after PAR treatment. Our results suggest that augmentation of central 5-HT neurotransmission has a beneficial effect on cardiovascular remodeling following volume overload. The mechanisms underlying this effect are unknown.
Agid:
5512539