Effect of melatonin on blood pressure and nitric oxide generation in rats with metabolic syndrome

Title:

Effect of melatonin on blood pressure and nitric oxide generation in rats with metabolic syndrome

Creator:

Klimentova, J., Cebova, M., Barta, A., Matuskova, Z., Vrankova, S., Rehakova, R., Kovacsova, M., and Pechanova, O.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:148df18d-cfb2-4c03-8502-7ed05fc6325a
uuid:148df18d-cfb2-4c03-8502-7ed05fc6325a

Subject:

Melatonin, MT1 receptors, Metabolic syndrome, Nitric oxide, Heart, Aorta, and Brain

Type:

article, model:article, and TEXT

Description:

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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:Suppl 3

Harvested from:

CDK

Metadata only:

false