Functional interaction of AT1 and AT2 receptors in fructose-induced insulin resistance and hypertension in rats

Vascular Angiotensin Type 1 Receptor Expression Is Associated with Vascular Dysfunction, Oxidative Stress and Inflammation in Fructose-Fed Rats

“…The mechanism underlying this increase is not known, but it may be a compensatory increase to help maintain blood pressure under these conditions. Blood pressure's dependence on the functional interaction of vascular AT1R and AT2R has been demonstrated in FFR, yet that study was indirect in that they used AT1R blockers rather than gene expression to show effects on blood pressure these rats (12). Increased expression of renal AT1R has also been associated with hyperinsulinemia in the Zucker obese rat, another model of insulin resistance (14).…”

“…Previous studies from our laboratory have shown that high insulin concentrations can stimulate the RAS and subsequent production of angiotensin II in cultured vascular smooth muscle cells (9,10). A fructose-fed rat study has shown that RAS inhibition with enalapril increases vascular endothelial nitric oxide synthase (eNOS) activity (11), and it can be argued that the angiotensin type 1 receptor (AT1R) is responsible for hypertension (12). However, it has yet to be demonstrated that gene expression of local vascular components of the RAS is increased in cardiovascular tissue from FFR, and this would be a necessary step in the implication of its role in hypertension.…”

Metabolic actions of angiotensin receptor antagonists: PPAR-γ agonist actions or a class effect?

“…Conversely, blockade of AT 1 receptors in insulin-resistant fructose-fed rats increased hepatic glucose output [24]. Thus, the actions of angiotensin II oppose those of glucagon [25].…”

Metabolic effects of excessive consumption of fructose

“…Doświadczenia na szczurach wykazały, iż dieta bogata w fruktozę może przyczyniać się do wzrostu ciśnienia [41,42]. Niektóre badania sugerują, iż opisywany efekt działa-nia fruktozy na wartości ciśnienia tętniczego krwi wynika nie bezpośrednio z wpływu fruktozy, a raczej występuje w związku z niedostateczną podażą magnezu lub miedzi w pożywieniu podawanym podczas badań [43,44].…”