J 2023

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

MCSWEENEY, Kristen Renee, Laura Kate GADANEC, Peter KUBATKA, Martin CAPRNA, Ludovit GASPAR et. al.

Basic information

Original name

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

Authors

MCSWEENEY, Kristen Renee (36 Australia), Laura Kate GADANEC (36 Australia), Peter KUBATKA (703 Slovakia), Martin CAPRNA (703 Slovakia), Ludovit GASPAR (703 Slovakia), Robert PROSECKÝ (203 Czech Republic, belonging to the institution), Delian DELEV (100 Bulgaria), Peter KRUŽLIAK (703 Slovakia, belonging to the institution), Vasso APOSTOLOPOULOS (36 Australia) and Anthony ZULLI (36 Australia, guarantor)

Edition

MOLECULAR AND CELLULAR BIOCHEMISTRY, NETHERLANDS, SPRINGER, 2023, 0300-8177

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10608 Biochemistry and molecular biology

Country of publisher

Germany

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 4.300 in 2022

RIV identification code

RIV/00216224:14110/23:00133476

Organization unit

Faculty of Medicine

UT WoS

001099394000023

Keywords in English

Angiotensin II; Angiotensin type 1 receptor; Angiotensin type 2 receptor; Cisplatin; Contraction; Renin angiotensin system
Změněno: 29/2/2024 13:41, Mgr. Tereza Miškechová

Abstract

V originále

The renin angiotensin system is a key regulator of blood pressure homeostasis. Angiotensin type 1 (AT1R) and 2 receptors (AT2R) have been investigated as targets for cisplatin-induced acute kidney injury; however, their therapeutic potential remains inconclusive. This pilot study aimed to determined the effect that acute cisplatin treatment had on angiotensin II (AngII)-induced contraction in blood vessels and expression profiles of AT1R and AT2R in mouse arteries and kidneys. Male C57BL/6 mice at 18 week of age (n = 8) were treated with vehicle or bolus dose of cisplatin (12.5 mg/kg). Thoracic aorta (TA), adnominal aorta (AA), brachiocephalic arteries (BC), iliac arteries (IL) and kidneys were collected for isometric tension and immunohistochemistry analysis. Cisplatin treatment reduced IL contraction to AngII at all doses (p < 0.01, p < 0.001, p < 0.0001); however, AngII did not induce contraction in TA, AA or BC in either treatment group. Following cisplatin treatment, AT1R expression was significantly upregulated in the media of TA (p < 0.0001) and AA (p < 0.0001), and in the endothelium (p < 0.05) media (p < 0.0001) and adventitia (p < 0.01) of IL. Cisplatin treatment significantly reduced AT2R expression in the endothelium (p < 0.05) and media (p < 0.05) of TA. In renal tubules, both AT1R (p < 0.01) and AT2R (p < 0.05) were increased following cisplatin treatment. Herein, we report that cisplatin reduces AngII-mediated contraction in IL and may be explained by an absence of normal counterregulatory expression of AT1R and AT2R, indicating other factors are involved.