Cisplatin-induced Nephrotoxicity Alters Blood Pressure Response to Angiotensin II Administration in Rats

Overview

Journal Adv Biomed Res

Specialty Biomedical Engineering

Date 2016 Apr 26

PMID 27110550

Citations 5

Authors

Aghdas Dehghani

Shadan Saberi

Mehdi Nematbakhsh

Affiliations

Soon will be listed here.

Abstract

Background: Cisplatin (CP) is an effective chemotherapeutic drug used in the clinic, which is accompanied with nephrotoxicity. CP may also disturb hemodynamics of the circulation system. We have tested the role of CP in mean arterial pressure (MAP) response to graded angiotensin (Ang) II infusion in rats.

Materials And Methods: Male and female rats were treated with CP (2.5 mg/kg/day) for a period of 1-week and compared with the vehicle-treated animals. The blood pressure response to Ang II (100-1000 ng/kg/min) was determined under the anesthesia condition. Endothelial permeability of aorta was measured according to the Evans blue uptake. The kidney tissue was also subjected to histological investigation.

Results: Significant increase in serum levels of blood urea nitrogen and creatinine and pathological findings in CP-treated rats verified CP-induced nephrotoxicity. Significant difference in percentage of change in MAP response to Ang II between male and female rats was detected in vehicle-treated groups (P < 0.05) while in CP-treated animals this response difference was not observed. The groups were not significantly different with regard to the endothelial permeability of aorta while the serum level of nitrite in male rats increased significantly following administration of CP (P < 0.05).

Conclusion: It seems the different response in percentage of change of MAP to graded Ang II infusion between male and female indicates the effect of CP on renin Ang system parameters.

Citing Articles

The Renin-Angiotensin System Involvement in Cisplatin-Induced Nephrotoxicity: An Overview of Physiological and Pathological Mechanisms-A Systematic Review.

Vakilian A, Mohammadi S, Shokri F, Maleki M, Kheiry M, Kheiri A Int J Nephrol. 2024; 2024:1511216.

PMID: 38799728 PMC: 11127762. DOI: 10.1155/2024/1511216.

Cisplatin treatment reduces contraction to angiotensin II by altering expression of angiotensin II receptors: a pilot study.

McSweeney K, Kate Gadanec L, Kubatka P, Caprnda M, Gaspar L, Prosecky R Mol Cell Biochem. 2023; 478(12):2907-2916.

PMID: 37004639 DOI: 10.1007/s11010-023-04706-2.

Protective Effect of Gamma Aminobutyric Acid against Aggravation of Renal Injury Caused by High Salt Intake in Cisplatin-Induced Nephrotoxicity.

Lee H, Ji S, Hwangbo H, Kim M, Kim D, Park B Int J Mol Sci. 2022; 23(1).

PMID: 35008928 PMC: 8745502. DOI: 10.3390/ijms23010502.

Perindopril regulates the inflammatory mediators, NF-κB/TNF-α/IL-6, and apoptosis in cisplatin-induced renal dysfunction.

Shalkami A, Hassan M, Abd El-Ghany A Naunyn Schmiedebergs Arch Pharmacol. 2018; 391(11):1247-1255.

PMID: 30066022 DOI: 10.1007/s00210-018-1550-0.

Nephroprotective efficacy of ceftriaxone against cisplatin-induced subchronic renal fibrosis in rats.

Abdel-Daim M, El-Sayed Y, Abd Eldaim M, Ibrahim A Naunyn Schmiedebergs Arch Pharmacol. 2016; 390(3):301-309.

PMID: 27975300 DOI: 10.1007/s00210-016-1332-5.

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