ArticleJournal of experimental pharmacology2025
Antihypertensive Effects of Diosmetin in Hypertension-Induced Cardiovascular Abnormalities in Rats.
Article in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Hypertension is associated with cardiovascular dysfunction and remodeling. Diosmetin, a flavonoid isolated from citrus seeds, has various biological properties. This work investigated the effects of diosmetin on cardiovascular parameters and classical and non-classical renin-angiotensin systems (RAS) in two-kidney one-clip (2K-1C) rats. Methods: 2K-1C hypertension was induced by placing a silver clip on the left renal artery. Three weeks after induction, rats were orally gavage with either vehicle, diosmetin (20 or 40 mg/kg), or telmisartan (5 mg/kg) for four weeks. Blood pressure (BP) was monitored weekly while vascular function and histomorphology studies were performed at the end of the study. Oxidative stress markers and RAS parameters, including serum angiotensin-converting enzyme (ACE) activity and plasma angiotensin II and angiotensin I-7 (Ang-(1-7)) concentrations, were also measured. The expression levels of angiotensin II type 1 receptor (AT Results: In this in vivo study on the 2K-1C rats, diosmetin exhibited antihypertensive effects in the 2K-1C model via modulation of the RAS. Diosmetin at doses of 20 and 40 mg/kg decreased BP by 11.73% and 23.17%, respectively. Diosmetin also improved vascular function by reducing sympathetic nerve-mediated vasoconstriction and restoring endothelium-mediated vasodilation in the mesentery and aortic rings. The thickening of the left ventricle and aorta in hypertensive rats was alleviated by diosmetin treatment. RAS parameters and oxidative stress markers were improved in the diosmetin-treated group compared to the untreated group. Additionally, diosmetin treatment restored the overexpression of the AT Conclusion: Diosmetin restored hemodynamic alterations associated with the improvement of vascular function. It also ameliorated left ventricular-aortic hypertrophy in hypertensive rats. These effects could be attributed to its capacity to modulate classical and non-classical RAS.
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