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Acute Angiotensin II Infusion Promotes Local Production of Prostaglandin E2 and Reactive Species in the Renal Cortex

Wael A.Alanazi Selim Fakhruddin Keith E. Jackson

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DOI: http://dx.doi.org/10.15520/ijmhs.2016.vol6.iss5.137.

Abstract


Angiotensin II (ANGII) is a systemic vasoconstrictor and body fluid regulator. Virtually all released ANGII binds to AT1 receptors, which stimulates cell signaling pathways in various cell types. In kidneys, ANGII enhances arachidonic acid release by increasing the activity of phospholipase enzymesand cyclooxygenase-2 (COX-2), leading to an elevation in prostaglandinlevels where prostaglandin E2 (PGE2) is predominately generated. Male Sprague Dawley rats (200 – 300g) were acutely injected for four hours by vehicle or ANGII (7ng/kg/min, IV). Blood pressure was elevated significantly during ANGII infusion from (109.82 ± 0.085mmHg) to (129.36 ± 0.1mmHg). Urine flow(8.98 ± 0.23μl/min), glomerular filtration rate (1.93 ± 0.18ml/min/gm), and renal blood flow(1.75 ± 0.064ml/min) were decreased in comparison with control(14.03 ± 0.26μl/min), (2.71 ± 0.075ml/min) and (3.8 ± 0.14ml/min/gm) respectively. Through renal microdialysis, we found that PGE2 levels were significantly induced by ANGII treatment (358.27 ± 35.3pg/ml)when compared to control(234.39 ± 11.72pg/ml).Also, acute ANGII infusion augmented the present oxidative stress in renal tissues. Superoxide and peroxynitrite levels were increased by two fold during ANGII treatment when evaluated by EPR using CMH and CPH as spin traps.In the current study, we found that local effects of acute ANGII infusion stimulate PGE2 and free reactive species, which produce a disruption in normal renal hemodynamic function. In summary, the present study demonstrates a potential mechanism by which acute elevations in ANGII promotes hypertension induced end organ kidney damage.


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