Facilitation of renal autoregulation by angiotensin II is mediated through modulation of nitric oxide

Guan, Z., Willgoss, D. A., Matthias, A., Manley, S. W., Crozier, S., Gobe, G. and Endre, Z. H. (2003) Facilitation of renal autoregulation by angiotensin II is mediated through modulation of nitric oxide. Acta Physiologica Scandinavica, 179 2: 189-201. doi:10.1046/j.1365-201X.2003.01125.x


Author Guan, Z.
Willgoss, D. A.
Matthias, A.
Manley, S. W.
Crozier, S.
Gobe, G.
Endre, Z. H.
Title Facilitation of renal autoregulation by angiotensin II is mediated through modulation of nitric oxide
Journal name Acta Physiologica Scandinavica   Check publisher's open access policy
ISSN 0001-6772
Publication date 2003-10-01
Sub-type Article (original research)
DOI 10.1046/j.1365-201X.2003.01125.x
Volume 179
Issue 2
Start page 189
End page 201
Total pages 13
Editor B. Uvnas
Place of publication Oxford, England
Publisher Blackwell Science
Collection year 2003
Language eng
Subject C1
321012 Nephrology and Urology
730115 Urogenital system and disorders
Abstract Aims: This study was designed to investigate the influence of angiotensin II (Ang II) and nitric oxide (NO) on autoregulation of renal perfusion. Methods: Autoregulation was investigated in isolated perfused kidneys (IPRK) from Sprague-Dawley rats during stepped increases in perfusion pressure. Results: Ang II (75-200 pM) produced dose-dependent enhancement of autoregulation whereas phenylephrine produced no enhancement and impaired autoregulation of GFR. Enhancement by Ang II was inhibited by the AT(1) antagonist, Losartan, and the superoxide scavenger, Tempol. Under control conditions nitric oxide synthase (NOS) inhibition by 10 muM N-omega-nitro-L-arginine methyl ester (L-NAME) facilitated autoregulation in the presence of non-specific cyclooxygenase (COX) inhibition by 10 muM indomethacin. Both COX and combined NOS/COX inhibition reduced the autoregulatory threshold concentration of Ang II. Facilitation by 100 pM Ang II was inhibited by 100 muM frusemide. Methacholine (50 nM) antagonised Ang II-facilitated autoregulation in the presence and absence of NOS/COX inhibition. Infusion of the NO donor, 1 muM sodium nitroprusside, inhibited L-NAME enhancement of autoregulation under control conditions and during Ang II infusion. Conclusions: The results suggest than an excess of NO impairs autoregulation under control conditions in the IPRK and that endogenous and exogenous NO, vasodilatory prostaglandins and endothelium-derived hyperpolarizing factor (EDHF) activity antagonise Ang II-facilitated autoregulation. Ang II also produced a counterregulatory vasodilatory response that included prostaglandin and NO release. We suggest that Ang II facilitates autoregulation by a tubuloglomerular feedback-dependent mechanism through AT(1) receptor-mediated depletion of nitric oxide, probably by stimulating generation of superoxide.
Keyword Physiology
Angiotensin Ii
Endothelium Derived Hyperpolarizing Factor
Erythrocyte Perfused Rat Kidney
Isolated Perfused Rat Kidney
Myogenic Response
Nitric Oxide
Phenylephrine
Renal Autoregulation
Tubuloglomerular Feedback
Blood-flow Autoregulation
Perfused Rat-kidney
Converting-enzyme-inhibition
Glomerular-filtration Rate
Protein-kinase-c
Hypertensive-rats
Relaxing Factor
Afferent
No
Q-Index Code C1

 
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Created: Tue, 14 Aug 2007, 19:19:11 EST