Objectives: 

Metabolic syndrome is characterized as a cluster of risk factors in which impaired nitric oxide-(NO)-dependent signaling pathways and icreased production of reactive oxygen species (ROS) were documented. Consequently, oxidative stress may lead to activation of nuclear factor kappa B (NFkB). The aim of this study was to determine NO and ROS generation as well as changes in blood pressure in two different models of metabolic syndrome (MS) represented by obese spontaneously hypertensive rats [SHR/ND mcr-cp (cp/cp)] and hereditary hypertriglyceridemic rats (HTG).

Materials: 

Animals were divided into four groups: male young 6-week-old normotensive control Wistar Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR), [SHR/ND mcr-cp (cp/cp)] and HTG rats. We measured blood pressure, nitric oxide synthase (NOS) activity, expression of endothelial NOS (eNOS) and NFkB in the heart, kidney and brain. Concentration of conjugated dienes (CD) and activity of superoxide dismutase (SOD) were measured in the same tissues.

Results: 

Blood pressure was significantly enhanced in SHR, SHR/ND mcr-cp (cp/cp), and HTG rats. NOS activity in the heart, kidney and brain was decreased in both models of MS. On the other hand, expression of eNOS protein was significantly increased in rats with MS in comparison with WKY. Similarly, expression of NFkB was increased in all tissues investigated. But increased concentration of CD along with decreased SOD activity were determined in HTG rats only.

Conclusions: 

Our data clearly showed elevated blood pressure and decreased NOS activity in the tissues of both models of metabolic syndrome. Since increased markers of oxidative stress were documented in HTG rats only, we hypothetised that other mechanisms, different from increased ROS production, might be responsible for incresed blood pressure and decreased NOS activity in the model of SHR/ND mcr-cp (cp/cp).

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