Subpressor doses of angiotensin II increase plasma F-2-isoprostanes in rats

Citation
Jf. Reckelhoff et al., Subpressor doses of angiotensin II increase plasma F-2-isoprostanes in rats, HYPERTENSIO, 35(1), 2000, pp. 476-479
Citations number
22
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194-911X → ACNP
Volume
35
Issue
1
Year of publication
2000
Part
2
Supplement
S
Pages
476 - 479
Database
ISI
SICI code
0194-911X(200001)35:1<476:SDOAII>2.0.ZU;2-T
Abstract
The present study was performed to determine whether physiologically releva nt doses of angiotensin II (Ang LT), which do not affect renal hemodynamics but do cause slow response hypertension, result in oxidative stress as mea sured by production of vasoconstrictor F-2-isoprostane, a prostaglandin-lik e non-cyclooxygenase-produced arachidonic acid metabolite that is the end p roduct of lipid peroxidation. Rats were instrumented with abdominal aortic and left femoral venous catheters, and before and throughout Ang TI (or sal ine) infusion, all rats received enalapril (250 mg/L). Four days after the initiation of enalapril, rats were infused with Ang II (10 ng . kg(-1) . mi n(-1), n=6) or saline. (n=6) for 14 days. Mean arterial pressure was measur ed 24 hours per day, and on day 12, glomerular filtration rate and renal pl asma flow were measured. Mean arterial pressure in control rats averaged 85 +/-1. mm Hg, and with Ang II infusion, mean arterial pressure increased slo wly and reached a plateau on day 3, averaging 117+/-2 mm Hg (P<0.0001 compa red with enalapril alone). Glomerular filtration rate and renal plasma flow were not affected by Ang II. Free F-2-isoprostanes in plasma increased by 54% with Ang II (P<0.01), and the production of F-2-isoprostanes esterified in plasma lipids tended to be higher with Ang II also but did not reach si gnificance (P=0.1). These studies suggest that low doses of Ang II are capa ble of producing oxidative stress in animals. Whether oxidative stress play s a causative role in Ang II-mediated slow-response hypertension or is seco ndary to the hypertension is not clear from these data and will require fur ther study.