Cardiovascular disease (CVD) is a major source of morbidity and mortality in the Western World. Premenopausal and estrogen-treated postmenopausal women have a lower incidence of CVD. It has been suggested that circulating endogenous estrogens are probably responsible for this protection. This study investigated the hypothesis that the reduction of endothelial permeability is responsible for cardioprotective effects of estrogen in hypertensive animals. Fourty-four rats were ovariectomized and divided into five groups: groups 1, 2 and 4 received DOCA-salt and groups 3 and 5 received normal saline (N/S) injection for four weeks. Then, in groups 4 and 5 the blood pressure was measured. Group 1 received estradiol valerate and in groups 2 and 3 continued with DOCA-salt and N/S injection for six weeks, respectively. Endothelial permeability was measured by Evans Blue extraction method. There was no significant difference in endothelial permeability in coronary circulation in estrogen-treated group and controls (12.97±2.32 vs. 9.96±1.01, respectively). Also, aortic endothelial permeability in DOCA-salt hypertensive rats did not change significantly after estrogen treatment (28.34±3.65 vs. 41.60±5.98). This study showed that the cardioprotective effects of estrogen in DOCA-salt hypertensive animals are not mediated by a reduction of endothelial permeability.
Melatonin, a multitasking indolamine, seems to be involved in a variety of physiological and metabolic processes via both receptor-mediated and receptor-independent mechanisms. The aim of our study was to find out whether melatonin can affectblood pressure (BP), nitric oxide synthase (NOS) activity, eNOS and nNOS protein expressions in rats with metabolic syndrome (SHR/cp). Rats were divided into four groups: 6-week-old male WKY andSHR/cp and age-matched WKY and SHR/cp treated with melatonin (10 mg/kg/day) for 3 weeks. BP was measured by tail-cuff plethysmography. NOS activity, eNOS and nNOS protein expressions were determined in the heart, aorta, brain cortex
and cerebellum. MT1 receptors were analyzed in the brain cortex
and cerebellum. In SHR/cp rats, BP was decreased after melatonin treatment. In the same group, melatonin did not affect NOS activity and eNOS protein expression in the heart and aorta, while it increased both parameters in the brain cortex and cerebellum. Interestingly, melatonin elevated MT1 protein expression in the cerebellum. Neuronal NOS protein expression was not changed within the groups. In conclusion, increased NOS activity/eNOS upregulation in particular brain regions may
contribute partially to BP decrease in SHR/cp rats after melatonin treatment. Participation of MT1 receptors in this melatonin action may be supposed.