(-)-Epicatechin Improves Vasoreactivity and Mitochondrial Respiration in Thermoneutral-Housed Wistar Rat Vasculature

• Published in: Nutrients Vol. 14; no. 5; p. 1097
• Main Authors: Chun, Ji Hye, Henckel, Melissa M, Knaub, Leslie A, Hull, Sara E, Pott, Greg B, Walker, Lori A, Reusch, Jane E-B, Keller, Amy C
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 05.03.2022; MDPI
• Subjects: Acids; Adenosine diphosphate; Animal models; Animals; Antibodies; Biological activity; Body temperature; Body weight; Ca2+/calmodulin-dependent protein kinase II; cardiovascular disease; Cardiovascular diseases; Catechin - metabolism; Catechin - pharmacology; Endothelium; eNOS; Epicatechin; Global health; Glucose; Kinases; Laboratories; Mitochondria; Mitochondria - metabolism; Nitric oxide; Phosphorylation; Physiology; Potassium; Public health; Rats; Rats, Wistar; Respiration; Room temperature; Signal Transduction; Sodium; vascular; Vasodilation; St Louis Missouri; United States > US; cardiovascular disease; vascular; eNOS
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu14051097

Cardiovascular disease (CVD) is a global health concern. Vascular dysfunction is an aspect of CVD, and novel treatments targeting vascular physiology are necessary. In the endothelium, eNOS regulates vasodilation and mitochondrial function; both are disrupted in CVD. (−)-Epicatechin, a botanical compound known for its vasodilatory, eNOS, and mitochondrial-stimulating properties, is a potential therapy in those with CVD. We hypothesized that (−)-epicatechin would support eNOS activity and mitochondrial respiration, leading to improved vasoreactivity in a thermoneutral-derived rat model of vascular dysfunction. We housed Wistar rats at room temperature or in thermoneutral conditions for a total of 16 week and treated them with 1mg/kg body weight (−)-epicatechin for 15 day. Vasoreactivity, eNOS activity, and mitochondrial respiration were measured, in addition to the protein expression of upstream cellular signaling molecules including AMPK and CaMKII. We observed a significant improvement of vasodilation in those housed in thermoneutrality and treated with (−)-epicatechin (p < 0.05), as well as dampened mitochondrial respiration (p < 0.05). AMPK and CaMKIIα and β expression were lessened with (−)-epicatechin treatment in those housed at thermoneutrality (p < 0.05). The opposite was observed with animals housed at room temperature supplemented with (−)-epicatechin. These data illustrate a context-dependent vascular response to (−)-epicatechin, a candidate for CVD therapeutic development.