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.Základní údaje
Originální název
Cisplatin treatment reduces contraction to angiotensin II by altering expression of angiotensin II receptors: a pilot study
Autoři
MCSWEENEY, Kristen Renee (36 Austrálie), Laura Kate GADANEC (36 Austrálie), Peter KUBATKA (703 Slovensko), Martin CAPRNA (703 Slovensko), Ludovit GASPAR (703 Slovensko), Robert PROSECKÝ (203 Česká republika, domácí), Delian DELEV (100 Bulharsko), Peter KRUŽLIAK (703 Slovensko, domácí), Vasso APOSTOLOPOULOS (36 Austrálie) a Anthony ZULLI (36 Austrálie, garant)
Vydání
MOLECULAR AND CELLULAR BIOCHEMISTRY, NETHERLANDS, SPRINGER, 2023, 0300-8177
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
10608 Biochemistry and molecular biology
Stát vydavatele
Německo
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 4.300 v roce 2022
Kód RIV
RIV/00216224:14110/23:00133476
Organizační jednotka
Lékařská fakulta
UT WoS
001099394000023
Klíčová slova anglicky
Angiotensin II; Angiotensin type 1 receptor; Angiotensin type 2 receptor; Cisplatin; Contraction; Renin angiotensin system
Změněno: 29. 2. 2024 13:41, Mgr. Tereza Miškechová
Anotace
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.