Tags

Type your tag names separated by a space and hit enter

Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats.
Acta Physiol Scand. 2004 Nov; 182(3):313-8.AP

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.

Authors+Show Affiliations

Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15491410

Citation

Badzyńska, B, et al. "Effect of Exogenous Angiotensin II On Renal Tissue Nitric Oxide and Intrarenal Circulation in Anaesthetized Rats." Acta Physiologica Scandinavica, vol. 182, no. 3, 2004, pp. 313-8.
Badzyńska B, Grzelec-Mojzesowicz M, Sadowski J. Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats. Acta Physiol Scand. 2004;182(3):313-8.
Badzyńska, B., Grzelec-Mojzesowicz, M., & Sadowski, J. (2004). Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats. Acta Physiologica Scandinavica, 182(3), 313-8.
Badzyńska B, Grzelec-Mojzesowicz M, Sadowski J. Effect of Exogenous Angiotensin II On Renal Tissue Nitric Oxide and Intrarenal Circulation in Anaesthetized Rats. Acta Physiol Scand. 2004;182(3):313-8. PubMed PMID: 15491410.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of exogenous angiotensin II on renal tissue nitric oxide and intrarenal circulation in anaesthetized rats. AU - Badzyńska,B, AU - Grzelec-Mojzesowicz,M, AU - Sadowski,J, PY - 2004/10/20/pubmed PY - 2005/2/3/medline PY - 2004/10/20/entrez SP - 313 EP - 8 JF - Acta physiologica Scandinavica JO - Acta Physiol Scand VL - 182 IS - 3 N2 - 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. SN - 0001-6772 UR - https://www.unboundmedicine.com/medline/citation/15491410/Effect_of_exogenous_angiotensin_II_on_renal_tissue_nitric_oxide_and_intrarenal_circulation_in_anaesthetized_rats_ L2 - https://doi.org/10.1111/j.1365-201X.2004.01364.x DB - PRIME DP - Unbound Medicine ER -