CONTINUOUS LIGHT EXPOSURE- AND L-NAME-INDUCED LEFT VENTRICULAR REMODELLING: INTERACTIONS WITH MELATONIN AND CAPTOPRIL: PP.29.155

Abstract

Objective: Blood pressure enhancement induced by continuous light exposure represents an attractive but rarely investigated model of experimental hypertension. Design and Method: The aim of our study was to show whether the combination of continuous light (24 h/day) exposure and chronic L-NAME treatment induces remodelling of the left ventricle and whether captopril or melatonin are able to modify these potential alterations. Six groups (n = 8/group) of 3-month old Wistar rats were treated for six weeks: control (untreated rats) (c), L-NAME-treated (40 mg/kg/day) (L), exposed to continuous light (24), L-NAME treated and exposed to continous light (L24), light-exposed-L-NAME rats which were treated with either captopril 100 mg/kg/day (L24C), or melatonin (10 mg/kg/24 h) (L24CM). Systolic blood pressure (SBP) was measured by tail-cuff method. Relative weight of the LV, endothelial nitric oxide synthase (eNOS) and angiotensin converting enzyme (ACE) expression in tissues, malondialdehyd (MD) concentration in plasma, and the level of hydroxyproline in collagenous protein fractions were measured. Results: SBP increase was prevented by both drugs investigated but more prominently by captopril in L24. Expression of eNOS was decreased in the aorta of L24 compared to controls and neither drug has improved it. Expression of ACE was increased in L24 and both drugs prevented this increase. Increased oxidative load, estimated by concentration of MD in plasma, was reduced by both drugs. Only captopril reduced LV hypertrophy in L24, while both captopril and melatonin reduced hydroxyproline concentration(captopril in soluble collagenous fraction and melatonin in insoluble collagenous fraction) of the LV. Conclusion: It is concluded that although melatonin - in comparison to captopril - did not prevented the increase of LV weight, both captopril and melatonin prevented LV fibrosis development. This protective effect of both drugs may be due to their antioxidative effect and by reducing the ACE expression.