Protective Role of Angiotensin II Type 1 Receptor Blocker on Short Time Effect of Oleic Acid Induced Lung and Kidney Injury

Ardeshir Talebi, Fatemeh Emami, Reza Biranvand, Zahra Moosavi, Kimia Ramtin, Soheil Sadeghi, Kimia Baghaei, Zahra Lak, Mehdi Nematbakhsh

Abstract


Backgrounds: Acute respiratory distress syndrome (ARDS) causes high mortality rate in clinic, and the pathogenesis of this syndrome may interact with renin angiotensin system (RAS) components. The main objective of this study was to determine the protective role of AT1R antagonist (losartan) on oleic acid (OA) induced ARDS and kidney injury.

Methods: The animal model of ARDS was performed by intravenous administration of 250 µl/kg oleic acid (OA). Male and female rats were subjected to received intravenously vehicle (saline, groups 1 and 4), OA (groups 2 and 5), or losartan (10 mg/kg) plus OA (groups 3 and 6), and six hour later, the measurements were performed.

Results: Co‑treatment of OA and losartan increased the serum levels of blood urea nitrogen significantly  (P  <  0.05) and creatinine insignificantly in both gender. However, the OA induced kidney damage was decreased by losartan significantly in male  (P  <  0.05) and insignificantly in female rats. In addition, co‑treatment of OA and losartan decreased lung water content significantly in male rats (P  <  0.05). Based on tissue staining, no significant difference in lung tissue damages were observed between the groups, however some exudate were observed in lung male rats treated with OA alone which were abolished by losartan.

Conclusions: Losartan may protect the kidney and lung against OA induced tissue injury in male rats. This protective action is not certain in female rats.


Keywords


Angiotensin II; injury; kidney; losartan; lung; oleic acid

Full Text:

PDF

References


Walkey AJ, Summer R, Ho V, Alkana P. Acute respiratory

distress syndrome: Epidemiology and management approaches.

Clin Epidemiol 2012;4:159‑69.

ARDS Definition Task Force, Ranieri VM, Rubenfeld GD,

Thompson BT, Ferguson ND, Caldwell E, et al. Acute

respiratory distress syndrome: The Berlin definition. JAMA

;307:2526‑33.

Gonçalves‑de‑Albuquerque CF, Silva AR, Burth P,

Castro‑Faria MV, Castro‑Faria‑Neto HC. Acute respiratory

distress syndrome: Role of oleic acid‑triggered lung injury

and inflammation. Mediators Inflamm 2015:260465. doi:

1155/2015/260465.

Máca J, Jor O, Holub M, Sklienka P, Burša F, Burda M, et al.

Past and Present ARDS mortality rates: A systematic review.

Respir Care 2017;62:113‑22.

Darmon M, Clec’h C, Adrie C, Argaud L, Allaouchiche B,

Azoulay E, et al. Acute respiratory distress syndrome and risk

of AKI among critically ill patients. Clin J Am Soc Nephrol

;9:1347‑53.

Moss M, Mannino DM. Race and gender differences in acute

respiratory distress syndrome deaths in the United States: An

analysis of multiple‑cause mortality data (1979‑1996). Crit Care

Med 2002;30:1679‑85.

Yilin Z, Yandong N, Faguang J. Role of angiotensin‑converting

enzyme (ACE) and ACE2 in a rat model of smoke inhalation

induced acute respiratory distress syndrome. Burns

;41:1468‑77.

Wösten‑van Asperen RM, Lutter R, Specht PA, Moll GN,

van Woensel JB, van der Loos CM, et al. Acute respiratory

distress syndrome leads to reduced ratio of ACE/ACE2 activities

and is prevented by angiotensin‑(1‑7) or an angiotensin II

receptor antagonist. J Pathol 2011;225:618‑27.

He X, Han B, Mura M, Xia S, Wang S, Ma T, et al.

Angiotensin‑converting enzyme inhibitor captopril prevents

oleic acid‑induced severe acute lung injury in rats. Shock

;28:106‑11.

Zambelli V, Bellani G, Borsa R, Pozzi F, Grassi A, Scanziani M,

et al. Angiotensin‑(1‑7) improves oxygenation, while reducing

cellular infiltrate and fibrosis in experimental acute respiratory

distress syndrome. Intensive Care Med Exp 2015;3:44.

Shen L, Mo H, Cai L, Kong T, Zheng W, Ye J, et al. Losartan

prevents sepsis‑induced acute lung injury and decreases

activation of nuclear factor kappaB and mitogen‑activated

protein kinases. Shock 2009;31:500‑6.

Raiden S, Nahmod K, Nahmod V, Semeniuk G, Pereira Y,

Alvarez C, et al. Nonpeptide antagonists of AT1 receptor for

angiotensin II delay the onset of acute respiratory distress

syndrome. J Pharmacol Exp Ther 2002;303:45‑51.

Moslemi F, Taheri P, Azimipoor M, Ramtin S, Hashemianfar M,

Momeni‑Ashjerdi A, et al. Effect of angiotensin II type 1 receptor

blockade on kidney ischemia/reperfusion; A gender‑related

difference. J Renal Inj Prev 2016;5:140‑3.

Safari T, Nematbakhsh M. Angiotensin 1‑7 receptor and angiotensin II receptor 2 blockades prevent the increased

serum and kidney nitric oxide levels in response to angiotensin

II administration: Gender‑related difference. Int J Prev Med

;4:311‑5.

McGuire BB, Watson RW, Pérez‑Barriocanal F, Fitzpatrick JM,

Docherty NG. Gender differences in the renin‑angiotensin and

nitric oxide systems: Relevance in the normal and diseased

kidney. Kidney Blood Press Res 2007;30:67‑80.

Sandberg K, Ji H. Sex and the renin angiotensin system:

Implications for gender differences in the progression of kidney

disease. Adv Ren Replace Ther 2003;10:15‑23.

Heeba GH. Angiotensin II receptor blocker, losartan, ameliorates

gentamicin‑induced oxidative stress and nephrotoxicity in rats.

Pharmacology 2011;87:232‑40.

Saleh S, Ain‑Shoka AA, El‑Demerdash E, Khalef MM. Protective

effects of the angiotensin II receptor blocker losartan on

cisplatin‑induced kidney injury. Chemotherapy 2009;55:399‑406.

Haghighi M, Nematbakhsh M, Talebi A, Nasri H, Ashrafi F,

Roshanaei K, et al. The role of angiotensin II receptor

(AT1) blockade in cisplatin‑induced nephrotoxicity in rats:

Gender‑related differences. Ren Fail 2012;34:1046‑51.

Nematbakhsh M, Ashrafi F, Safari T, Talebi A, Nasri H,

Mortazavi M, et al. Administration of vitamin E and losartan as

prophylaxes in cisplatin‑induced nephrotoxicity model in rats.

J Nephrol 2012;25:410‑7.

Ashrafi F, Nematbakhsh M, Safari T, Talebi A, Nasri H,

Khazaei M, et al. A combination of vitamin C and losartan

for cisplatin‑induced nephrotoxicity in rats. Iran J Kidney Dis

;6:361‑5.

Akella A, Sharma P, Pandey R, Deshpande SB. Characterization

of oleic acid‑induced acute respiratory distress syndrome model

in rat. Indian J Exp Biol 2014;52:712‑9.

Elewa HA. Study the nephro‑protective effects of losartan on

rats. Int J Clin Pharmacol Pharmacother 2016;1:101.

Kennedy MT, Higgins BD, Costello JF, Curtin WA, Laffey JG.

Hypertonic saline redu injury. BMC Pulm Med 2008;8:9.

Vaidya VS, Ferguson MA, Bonventre JV. Biomarkers of acute

kidney injury. Annu Rev Pharmacol Toxicol 2008;48:463‑93.

Petretta M, Spinelli L, Marciano F, Apicella C, Vicario ML,

Testa G, et al. Effects of losartan treatment on cardiac autonomic

control during volume loading in patients with DCM. Am J

Physiol Heart Circ Physiol 2000;279:H86‑92.

Holtkamp FA, de Zeeuw D, Thomas MC, Cooper ME,

de Graeff PA, Hillege HJ, et al. An acute fall in estimated

glomerular filtration rate during treatment with losartan predicts

a slower decrease in long‑term renal function. Kidney Int

;80:282‑7.

de P Rodrigues SF, dos Santos RA, Silva‑Antonialli MM,

Scavone C, Nigro D, Carvalho MH, et al. Differential effect of

losartan in female and male spontaneously hypertensive rats.

Life Sci 2006;78:2280‑5.

Gheitasi I, Moosavi SM. Combination therapy with losartan

and α‑tocopherol in acute ureteral obstruction‑induced renal

excretory dysfunction and acidification defect. Iran J Med Sci

;39:357‑66.

Chen H, Zhou CH, Yang J. A modified rat model of

exercise‑induced renal injury and the protective effects of

losartan and yishen huanji decoction. Ren Fail 2013;35:951‑7.

Mihailovic‑Stanojevic N, Jovovic D, Miloradovic Z,

Grujic‑Milanovic J, Jerkic M, Markovic‑Lipkovski J. Reduced

progression of adriamycin nephropathy in spontaneously

hypertensive rats treated by losartan. Nephrol Dial Transplant

;24:1142‑50.

Vrigkou E, Tsangaris I, Bonovas S, Tsantes A, Kopterides P.

The evolving role of the renin‑angiotensin system in ARDS. Crit

Care 2017;21:329.

He X, Han B, Mura M, Xia S, Wang S, Ma T, et al.

Angiotensin‑converting enzyme inhibitor captopril prevents

oleic acid‑induced severe acute lung injury in rats. Shock

;28:106‑11.

Liu H, Zhang D, Zhao B, Zhao J. Superoxide anion, the main

species of ROS in the development of ARDS induced by oleic

acid. Free Radic Res 2004;38:1281‑7.

Ivanov M, Mihailović‑Stanojević N, Grujić Milanović J,

Jovović Đ, Marković‑Lipkovski J, Ćirović S, et al. Losartan

improved antioxidant defense, renal function and structure of

postischemic hypertensive kidney. PLoS One 2014;9:e96353.

Kamper M, Tsimpoukidi O, Chatzigeorgiou A, Lymberi M,

Kamper EF. The antioxidant effect of angiotensin II receptor

blocker, losartan, in streptozotocin‑induced diabetic rats. Transl

Res 2010;156:26‑36.

Argani H, Ghorbanihaghjo A, Aghaeishahsavari M,

Noroozianavval M, Rashtchizadeh N, Veisi P, et al. Effects of

losartan and enalapril on high‑sensitivity C‑reactive protein

and total antioxidant in renal transplant recipients with

Renin‑Angiotensin system polymorphisms. Transplant Proc

;40:16‑21.

Rao N, Moran CA. Pulmonary pathology: Acute lung injury.

st ed. New York: Demos Medical Publishing; 2014. p. 31‑4.

Gonçalves‑de‑Albuquerque CF, Silva AR, Burth P, de Moraes IM,

Oliveira FM, Younes‑Ibrahim M, et al. Oleic acid induces lung

injury in mice through activation of the ERK pathway. Mediators

Inflamm 2012;2012:956509. doi: 10.1155/2012/956509.