(-)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period

This study investigated the effects of (−)-epicatechin (Epi) in young male borderline hypertensive rats (BHR) during two weeks of treatment (Epi group, 100 mg/kg/day p.o.) and two weeks post treatment (PE group). Epi reduced blood pressure (BP), which persisted for two weeks post treatment. This was...

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Autori principali: Michal Kluknavsky (Autore), Peter Balis (Autore), Martin Skratek (Autore), Jan Manka (Autore), Iveta Bernatova (Autore)
Natura: Libro
Pubblicazione: MDPI AG, 2020-01-01T00:00:00Z.
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Riassunto:This study investigated the effects of (−)-epicatechin (Epi) in young male borderline hypertensive rats (BHR) during two weeks of treatment (Epi group, 100 mg/kg/day p.o.) and two weeks post treatment (PE group). Epi reduced blood pressure (BP), which persisted for two weeks post treatment. This was associated with delayed reduction of anxiety-like behaviour. Epi significantly increased nitric oxide synthase (NOS) activities in the aorta and left heart ventricle (LHV) vs. the age-matched controls without affecting the brainstem and frontal neocortex. Furthermore, Epi significantly reduced the superoxide production in the aorta and relative content of iron-containing compounds in blood. Two weeks post treatment, the NOS activities and superoxide productions in the heart and aorta did not differ from the age-matched controls. The gene expressions of the NOSs (<i>nNOS</i>, <i>iNOS</i>, <i>eNOS</i>), nuclear factor erythroid 2-related factor 2 (<i>Nrf2</i>), and peroxisome proliferator-activated receptor-γ (<i>PPAR</i>-γ) remained unaltered in the aorta and LHV of the Epi and PE groups. In conclusion, while Epi-induced a decrease of the rats’ BP persisted for two weeks post treatment, continuous Epi treatments seem to be necessary for maintaining elevated NO production as well as redox balance in the heart and aorta without changes in the <i>NOSs</i>, <i>Nrf2</i>, and <i>PPAR</i>-γ gene expressions.
Descrizione del documento:2076-3921
10.3390/antiox9020096