Enhanced Na⁺, K⁺-ATPase activity and endothelial modulation decrease phenylephrine-induced contraction in aorta from ouabain-treated normotensive and hypertensive rats

Abstract

The results suggest that long-term ouabain treatment reduces the α-adrenergic response of aorta from normotensive rats and SHRs, associated with an increase of NO synthesis, reduced COX-2-derived vasoconstrictor factors, and enhanced ouabain-sensitive Na+, K+-ATPase activity. These aortic mechanisms could be adjustments to the elevated blood pressure induced by ouabain, even in the presence of preexisting hypertension.

Cyclooxygenase-2 is a critical determinant of angiotensin II-induced vascular remodeling and stiffness in resistance arteries of ouabain-treated rats

“…High-serum endogenous ouabain level has been found in different models of hypertension [deoxycorticosterone acetate (DOCA)-salt, reduced renal mass, and Milan rats] [1][2][3] as well as in patients with essential hypertension [4,5]. Furthermore, normotensive rats receiving ouabain for 5 weeks (at doses to achieve a serum concentration like that found in essential hypertensive patients) develop higher blood pressure compared with that observed in patients with mild-to-moderate hypertension [6][7][8][9][10][11][12][13].…”

“…Over the last 20 years, our group and others have investigated the relationship between ouabain and arterial function. Specifically, three main hallmarks in the vasculature of 5-week ouabain-treated rats have been reported: diminished or unchanged adrenergic-mediated contraction in large and small arteries, with changes in the basal balance of endothelium-derived factors [7][8][9][11][12][13]14,15]; decreased vasoconstrictor response because of stimulation of perivascular innervation in mesenteric artery [16]; and unaltered endothelium-mediated vasodilation by acetylcholine in large and small arteries [8,14,15,17]. Collectively, these data strengthen the idea that functional vascular adjustments resulting from ouabain exposure for 5-week act as a mechanism to prevent the worsening of hypertension and not as a mechanism contributing to blood pressure elevation in rats.…”

Sardine proteins (Sardina pilchardus) combined with green lemon zest (Citrus latifolia) improve blood pressure, lipid profile and redox status in diabetic hypertensive rats

“…Diabetes mellitus and hypertension were enhanced oxidative stress and changes antioxidant capacity (Yang et al, 2011;Kapuku et al, 2016). Several reports had shown that the chronic administration of ouabain to Wistar rats induces hypertension (You et al, 2014;Davel et al, 2014). This hypertension seems to be depending, at least in part, on an activation of the central nervous mechanisms associated with increased sympathetic tone, subsequent to the activation of the brain reninangiotensin and endothelin systems (Di Filippo et al, 2003).…”