We are analyzing https://link.springer.com/article/10.1007/s11906-000-0078-z.

Title:
Free radical production and angiotensin | Current Hypertension Reports
Description:
Angiotensin II (ANG II) has multiple effects on cardiovascular and renal cells, including vasoconstriction, cell growth, induction of proinflammatory cytokines, and profibrogenic actions. Recent studies provide evidence that ANG II could stimulate intracellular formation of reactive oxygen species (ROS) such as the superoxide anion (O2 -). This ANG II-mediated ROS formation exhibits different kinetic and lower absolute concentrations than those traditionally observed during the respiratory burst of phagocytic cells, but it likely involves similar membrane-bound NAD(P)Hoxidases. Current evidence suggests that ANG II, through AT1-receptor activation, upregulates several subunits of this multienzyme complex, resulting in an increase in intracellular O2-concentration. ROS are involved in several signal pathways, and redox-sensitive transcriptional factors (AP-1, NF-kB) have been characterized. ANG II-induced ROS play a pivotal role in several pathophysiologic situations of vascular and renal cells such as hypertension, endothelial dysfunction, nitrate tolerance, atherosclerosis, and cellular remodeling. Although these perceptions suggest that drugs interfering with ANG II effects (ACE inhibitors, AT1 -receptor antagonist) may serve as antioxidants, preventing vascular and renal changes, the clinical studies are not so straightforward. In fact, only specific risk groups, such as patients with diabetes mellitus or renal insufficiency, may benefit from ACE inhibitors, whereas hard endpoints showed no advantage for ACE inhibitors in patients with essential hypertension.
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Topics {✒️}

cyclin/cyclin-dependent kinase complexes angiotensin-converting-enzyme inhibition compared renin-angiotensin system month download article/chapter proximal tubular cells reactive oxygen species respiratory burst mitogen-activated protein kinases activated oxygen species oxygen-derived free radicals stimulate intracellular formation receptor-mediated peroxide production redox-sensitive transcriptional factors nf-kb transcription factor oxidase-mediated superoxide production angiotensin ii-mediated expression reactive oxygen intermediates free radical production nadh/ nadph oxidase-derived quiescent balb/3t3 cells angiotensin ii-mediated hypertension oxidative stress-mediated activation proto-oncogenes c-fos proto-oncogenes c-myc cell growth cell cycle regulation angiotensin ii-induced tubular mct cells related subjects superoxide anion radical reactive oxygen full article pdf oxidant stress induces nadh/nadph oxidase privacy choices/manage cookies angiotensin ii type nadph oxidase activity catecholamine-induced hypertension acute simultaneous stimulation nice review discussing goldschmidt-clermont pj extracellular superoxide dismutase current evidence suggests article wolf mitogenic signaling mediated cell injury rabbit aortic adventitia nitric oxide synthases p22phox mrna expression human endothelial cells

Questions {❓}

Kumar KV, Das UN: Are free radicals involved in the pathobiology of human essential hypertension?

Schema {🗺️}

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         description:Angiotensin II (ANG II) has multiple effects on cardiovascular and renal cells, including vasoconstriction, cell growth, induction of proinflammatory cytokines, and profibrogenic actions. Recent studies provide evidence that ANG II could stimulate intracellular formation of reactive oxygen species (ROS) such as the superoxide anion (O2 -). This ANG II-mediated ROS formation exhibits different kinetic and lower absolute concentrations than those traditionally observed during the respiratory burst of phagocytic cells, but it likely involves similar membrane-bound NAD(P)Hoxidases. Current evidence suggests that ANG II, through AT1-receptor activation, upregulates several subunits of this multienzyme complex, resulting in an increase in intracellular O2-concentration. ROS are involved in several signal pathways, and redox-sensitive transcriptional factors (AP-1, NF-kB) have been characterized. ANG II-induced ROS play a pivotal role in several pathophysiologic situations of vascular and renal cells such as hypertension, endothelial dysfunction, nitrate tolerance, atherosclerosis, and cellular remodeling. Although these perceptions suggest that drugs interfering with ANG II effects (ACE inhibitors, AT1 -receptor antagonist) may serve as antioxidants, preventing vascular and renal changes, the clinical studies are not so straightforward. In fact, only specific risk groups, such as patients with diabetes mellitus or renal insufficiency, may benefit from ACE inhibitors, whereas hard endpoints showed no advantage for ACE inhibitors in patients with essential hypertension.
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