Objectives: 

Melatonin, a multitasking indolamine, seems to be involved in a variety of physiologic and metabolic processes via both receptor-mediated and receptor-independent mechanisms. The aim of this study was to find out whether melatonin can affect blood pressure, nitric oxide synthase (NOS) and superoxide dismutase (SOD) activities, protein expressions of eNOS and SOD, gene expressions of eNOS and SOD mRNA, and reduced gluthione (GSH) level in rats with metabolic syndrome (MS) - obese spontaneously hypertensive rats [SHR/ND mcr-cp (cp/cp)] and their normotensive control – Wistar Kyoto (WKY) and hypertensive control - spontaneously hypertensive rats (SHR).

Materials: 

Rats were divided into four groups: the first three groups represented male 6-week-old SHR, WKY, and rats with MS. The fourth group consisted of 6-week-old rats with MS which were treated with melatonin (10 mg/kg/day) for 3 weeks. We measured blood pressure, NOS activity in the heart and kidney, gene expression by real-time PCR and protein expression by Western blot analysis. Finally, concentration of thiol groups was determined in the kidney.

Results: 

In the rats with MS, blood pressure was decreased by 10% in comparison with age-matched untreated MS rats. There were no significant changes in upregulations of both NOS or SOD among the groups in the heart. In the kidney, NOS activity was decreased significantly in MS rats comparing to the WKY or SHR. Despite a remarcable increase in eNOS mRNA upregulation, melatonin had not yet increasing effect on NOS activity in the kidney. Interestingly, SOD activity in the plasma was not changed significantly among the groups, however, melatonin treatment increased this activity significantly by 50%.

Conclusions: 

The antioxidant effect which refers to the SOD activity, rather than increased NOS activity, was responsible for blood pressure reduction after melatonin treatment.

Supported by grants APVV-0538-07, APVV-0742-10 and VEGA: 2/0190/11, 2/0178/09.