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The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats

BACKGROUND: Nitric oxide (NO) as a vasodilator factor has renoprotective effect against renal ischemia. The balance between angiotensin II (Ang II) and NO can affect kidney homeostasis. The aim of this study was to determine NO alteration in response to renin–Ang system vasodilator receptors antagon...

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Autores principales: Maleki, Maryam, Hasanshahi, Jalal, Moslemi, Fatemeh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841005/
https://www.ncbi.nlm.nih.gov/pubmed/29531923
http://dx.doi.org/10.4103/2277-9175.225596
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author Maleki, Maryam
Hasanshahi, Jalal
Moslemi, Fatemeh
author_facet Maleki, Maryam
Hasanshahi, Jalal
Moslemi, Fatemeh
author_sort Maleki, Maryam
collection PubMed
description BACKGROUND: Nitric oxide (NO) as a vasodilator factor has renoprotective effect against renal ischemia. The balance between angiotensin II (Ang II) and NO can affect kidney homeostasis. The aim of this study was to determine NO alteration in response to renin–Ang system vasodilator receptors antagonists (PD123319; Ang II type 2 receptor antagonist and A779; Mas receptor antagonist) in renal ischemia/reperfusion injury (IRI) in rats. MATERIALS AND METHODS: Sixty-three Wistar male and female rats were used. Animals from each gender were divided into four groups received saline, Ang II, PD123319 + Ang II, and A779 + Ang II after renal IRI. Renal IRI induced with an adjustable hook. Blood pressure and renal blood flow (RBF) measured continuously. The nitrite levels were measured in serum, kidney, and urine samples. RESULTS: In female rats, the serum and kidney nitrite levels increased significantly by Ang II (P < 0.05) and decreased significantly (P < 0.05) when PD123319 was accompanied with Ang II. Such observation was not seen in male. Ang II decreased RBF significantly in all groups (P < 0.05), while PD + Ang II group showed significant decrease in RBF in comparison with the other groups in female rats (P < 0.05). CONCLUSION: Males show more sensibility to Ang II infusion; in fact, it is suggested that there is gender dimorphism in the Ang II and NO production associated with vasodilator receptors.
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spelling pubmed-58410052018-03-12 The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats Maleki, Maryam Hasanshahi, Jalal Moslemi, Fatemeh Adv Biomed Res Original Article BACKGROUND: Nitric oxide (NO) as a vasodilator factor has renoprotective effect against renal ischemia. The balance between angiotensin II (Ang II) and NO can affect kidney homeostasis. The aim of this study was to determine NO alteration in response to renin–Ang system vasodilator receptors antagonists (PD123319; Ang II type 2 receptor antagonist and A779; Mas receptor antagonist) in renal ischemia/reperfusion injury (IRI) in rats. MATERIALS AND METHODS: Sixty-three Wistar male and female rats were used. Animals from each gender were divided into four groups received saline, Ang II, PD123319 + Ang II, and A779 + Ang II after renal IRI. Renal IRI induced with an adjustable hook. Blood pressure and renal blood flow (RBF) measured continuously. The nitrite levels were measured in serum, kidney, and urine samples. RESULTS: In female rats, the serum and kidney nitrite levels increased significantly by Ang II (P < 0.05) and decreased significantly (P < 0.05) when PD123319 was accompanied with Ang II. Such observation was not seen in male. Ang II decreased RBF significantly in all groups (P < 0.05), while PD + Ang II group showed significant decrease in RBF in comparison with the other groups in female rats (P < 0.05). CONCLUSION: Males show more sensibility to Ang II infusion; in fact, it is suggested that there is gender dimorphism in the Ang II and NO production associated with vasodilator receptors. Medknow Publications & Media Pvt Ltd 2018-02-16 /pmc/articles/PMC5841005/ /pubmed/29531923 http://dx.doi.org/10.4103/2277-9175.225596 Text en Copyright: © 2018 Advanced Biomedical Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Maleki, Maryam
Hasanshahi, Jalal
Moslemi, Fatemeh
The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title_full The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title_fullStr The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title_full_unstemmed The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title_short The Role of Vasodilator Receptors of Renin–angiotensin System on Nitric Oxide Formation and Kidney Circulation after Angiotensin II Infusion in Renal Ischemia/Reperfusion Rats
title_sort role of vasodilator receptors of renin–angiotensin system on nitric oxide formation and kidney circulation after angiotensin ii infusion in renal ischemia/reperfusion rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841005/
https://www.ncbi.nlm.nih.gov/pubmed/29531923
http://dx.doi.org/10.4103/2277-9175.225596
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