Angiotensin II facilitates autoregulation in the perfused mouse kidney: An optimized in vitro model for assessment of renal vascular and tubular function

Rahgozar, M, Guan, ZG, Matthias, A, Gobe, GC and Endre, ZH (2004) Angiotensin II facilitates autoregulation in the perfused mouse kidney: An optimized in vitro model for assessment of renal vascular and tubular function. Nephrology, 9 5: 288-296. doi:10.1111/j.1440-1797.2004.00316.x


Author Rahgozar, M
Guan, ZG
Matthias, A
Gobe, GC
Endre, ZH
Title Angiotensin II facilitates autoregulation in the perfused mouse kidney: An optimized in vitro model for assessment of renal vascular and tubular function
Journal name Nephrology   Check publisher's open access policy
ISSN 1320-5358
Publication date 2004
Sub-type Article (original research)
DOI 10.1111/j.1440-1797.2004.00316.x
Volume 9
Issue 5
Start page 288
End page 296
Total pages 9
Editor D. C. H. Harris
Place of publication Carlton South, Australia
Publisher Blackwell Publishing Asia
Collection year 2004
Language eng
Subject C1
321012 Nephrology and Urology
730115 Urogenital system and disorders
Abstract Background and Aims: We have optimized the isolated perfused mouse kidney (IPMK) model for studying renal vascular and tubular function in vitro using 24-28 g C57BL6J mice; the wild type controls for many transgenic mice. Methods and Results: Buffer composition was optimized for bovine serum albumin concentration (BSA). The effect of adding erythrocytes on renal function and morphology was assessed. Autoregulation was investigated during stepped increases in perfusion pressure. Perfusion for 60 min at 90-110 mmHg with Krebs bicarbonate buffer containing 5.5% BSA, and amino acids produced functional parameters within the in vivo range. Erythrocytes increased renal vascular resistance (3.8 +/- 0.2 vs 2.4 +/- 0.1 mL/min.mmHg, P < 0.05), enhanced sodium reabsorption (FENa = 0.3 +/- 0.08 vs 1.5 +/- 0.7%, P < 0.05), produced equivalent glomerular filtration rates (GFR; 364 +/- 38 vs 400 +/- 9 muL/min per gkw) and reduced distal tubular cell injury in the inner stripe (5.8 +/- 1.7 vs 23.7 +/- 3.1%, P < 0.001) compared to cell free perfusion. The IPMK was responsive to vasoconstrictor (angiotensin II, EC50 100 pM) and vasodilator (methacholine, EC50 75 nM) mediators and showed partial autoregulation of perfusate flow under control conditions over 65-85 mmHg; autoregulatory index (ARI) of 0.66 +/- 0.11. Angiotensin II (100 pM) extended this range (to 65-120 mmHg) and enhanced efficiency (ARI 0.21 +/- 0.02, P < 0.05). Angiotensin II facilitation was antagonized by methacholine (ARI 0.76 +/- 0.08) and papaverine (ARI 0.91 +/- 0.13). Conclusion: The IPMK model is useful for studying renal physiology and pathophysiology without systemic neurohormonal influences.
Keyword Urology & Nephrology
Angiotensin Ii
Autoregulation
Erythrocytes
Medullary Hypoxia
Methacholine
Mouse Kidney
Thick Ascending Limb
Rat-kidney
Nitric-oxide
Hypoxic Injury
Intact Kidney
Knockout Mice
Oxygen
Modulation
Damage
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
2005 Higher Education Research Data Collection
School of Medicine Publications
 
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Created: Wed, 15 Aug 2007, 03:32:50 EST