0000000000315819
AUTHOR
Veronica Azcutia
Complete blockade of the vasorelaxant effects of angiotensin-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas
Key points • Two distinct angiotensin-(1–7) [Ang-(1–7)] receptor blockers, A779 and d-Pro-Ang-(1–7), can completely prevent Ang-(1–7)-induced vasorelaxation. • Genetic deficiency of Mas completely prevents vascular responses to Ang-(1–7). • Genetic deficiency of Mas completely prevents vascular responses to other NO-dependent vasorelaxants (bradykinin). • Mas plays a key role in NO-mediated vasodilatation by modulating vasorelaxant-mediated phosphorylation of endothelial nitric oxide synthase in endothelial cells. Abstract The heptapeptide angiotensin-(1–7) is a biologically active metabolite of angiotensin II, the predominant peptide of the renin–angiotensin system. Recently, we have show…
Inflammation Determines the Pro-Adhesive Properties of High Extracellular D-Glucose in Human Endothelial Cells In Vitro and Rat Microvessels In Vivo
BACKGROUND: Hyperglycemia is acknowledged as an independent risk factor for developing diabetes-associated atherosclerosis. At present, most therapeutic approaches are targeted at a tight glycemic control in diabetic patients, although this fails to prevent macrovascular complications of the disease. Indeed, it remains highly controversial whether or not the mere elevation of extracellular D-glucose can directly promote vascular inflammation, which favors early pro-atherosclerotic events. METHODS AND FINDINGS: In the present work, increasing extracellular D-glucose from 5.5 to 22 mmol/L was neither sufficient to induce intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion mo…