Abstract
The renin-angiotensin-aldosterone system (RAAS) is a dominant player in several cardiovascular pathologies. This study investigated whether alterations induced by l-NAME, (NLG)-nitro-l-arginine methyl ester, a nitric oxide synthase inhibitor, and the protective effect of melatonin are associated with changes in the RAAS. Four groups of 3-month-old male Wistar rats (n = 10) were treated as follows for four weeks: untreated controls, rats treated with melatonin (10 mg/kg/day), rats treated with l-NAME (40 mg/kg/day), and rats treated with l-NAME + melatonin. l-NAME administration led to hypertension and left ventricular (LV) fibrosis in terms of enhancement of soluble, insoluble and total collagen concentration and content. Melatonin reduced systolic blood pressure enhancement and lowered the concentration and content of insoluble and total collagen in the LV. The serum concentration of angiotensin (Ang) 1–8 (Ang II) and its downstream metabolites were reduced in the l-NAME group and remained unaltered by melatonin. The serum aldosterone level and its ratio to Ang II (AA2-ratio) were increased in the l-NAME group without being modified by melatonin. We conclude that l-NAME-hypertension is associated with reduced level of Ang II and its downstream metabolites and increased aldosterone concentration and AA2-ratio. Melatonin exerts its protective effect in l-NAME-induced hypertension without affecting RAAS.
Highlights
Nitric oxide (NO) provides cardiovascular protection by reducing blood pressure and via its antiproliferative and antifibrotic actions [1,2]
Melatonin deficiency induced by experimental pinealectomy or continuous melatonin deficiency induced by experimental pinealectomy or continuous light exposure in rats results light in rats results in theand development of hypertension and myocardial fibrosis in theexposure development of hypertension myocardial fibrosis
We did not measure the parameters characterizing NO-production in the current study, our previous experiments indicate that blood pressure reduction by melatonin and its antiremodeling effect may be associated with the improvement of endothelial function in
Summary
Nitric oxide (NO) provides cardiovascular protection by reducing blood pressure and via its antiproliferative and antifibrotic actions [1,2]. Melatonin deficiency induced by experimental pinealectomy or continuous melatonin deficiency induced by experimental pinealectomy or continuous light exposure in rats results light in rats results in theand development of hypertension and myocardial fibrosis [13,14]. The pathomechanism melatonin protection seems be highlyof complex. The activation of protection seems to beofhighly complex. Of data on the ability of amelatonin of on the ability of melatonin to interfere with neurohumoral activation, with the to data interfere with neurohumoral activation, with the RAAS in variable cardiovascular. RAAS in variable cardiovascular of the current study was to test whether pathologies.
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