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Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats

B. Bądzyńska

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

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M. Grzelec‐Mojzesowicz

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

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J. Sadowski

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

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First published: 19 October 2004
Cited by: 7
J. Sadowski, Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5, PL02‐106 Warsaw, Poland.

Abstract

Aim: The renal medullary circulation is protected against depressor action of angiotensin II (Ang II) because of the opposed action of a vasodilator agent, possibly nitric oxide (NO). This possibility was evaluated by a simultaneous determination of the effect of exogenous Ang II on renal cortical and medullary tissue NO and on intrarenal circulation.

Methods: In anaesthetized rats effects were determined of pressor and subpressor Ang II doses on tissue NO concentration in the renal cortex and inner medulla (selective NO electrodes), total renal blood flow (RBF, Transonic renal artery probe) and inner medullary blood flow (IMBF, laser Doppler flux). The measurements were repeated in rats treated with tempol, a scavenger of superoxide.

Results: Moderately pressor Ang II infusion significantly decreased tissue NO signal from 5.7 ± 0.2 to 5.3 ± 0.2 nA in the cortex and from 10.7 ± 0.6 to 10.1 ± 0.6 nA in the medulla. The RBF, a measure of cortical perfusion, decreased, and IMBF did not change. Subpressor doses of Ang II did not change medullary or cortical tissue NO. Tempol prevented an Ang II dependent decrease in medullary (but not cortical) NO without affecting RBF or IMBF responses.

Conclusion: An absence of an increase in renal cortical or medullary tissue NO after infusion of subpressor or pressor doses of Ang II speaks against the role of this agent in buffering the intrarenal vasoconstrictor action of the hormone. Elimination of the post‐Ang II decrease in medullary NO in animals pre‐treated with tempol suggests that tissue superoxide generation stimulated by the hormone might reduce local bioavailability of NO.

Number of times cited: 7

  • , Role of l-arginine uptake mechanisms in renal blood flow responses to angiotensin II in rats, Acta Physiologica, 203, 3, (391), (2011).
  • , Angiotensin II and neurohumoral control of the renal medullary circulation, Clinical and Experimental Pharmacology and Physiology, 37, 2, (e58-e69), (2009).
  • , NADPH-d cells (mast cells) around and within the autonomic nerves of porcine renal hilus, Tissue and Cell, 42, 3, (195), (2010).
  • , Protective effects of antioxidant-fortified diet on renal function and metabolic profile in obese Zucker rat, Endocrine, 35, 1, (89), (2009).
  • , Mitochondrial function and nitric oxide metabolism are modified by enalapril treatment in rat kidney, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 292, 4, (R1494), (2007).
  • , Renal hemodynamic responses to intrarenal infusion of acetylcholine: Comparison with effects of PGE2 and NO donor, Kidney International, 69, 10, (1774), (2006).
  • , Different effects of pentobarbital and pentylenetetrazol on nitric oxide levels in rat frontal cortex, Acta veterinaria, 55, 5-6, (367), (2005).