Angiotensin II type 1 receptor is involved in hypertension and vascular alterations caused by environmental toxicant hexachlorobenzene. (2021)

• Record Type: Journal Article
• Authors: Romero Caimi, Giselle; Gorzalczany, Susana; Bonazzola, Patricia; Deza, Zahira; Rosón, María Inés; Alvarez, Laura; Castilla, Rocío
• Is Part Of: Toxicology reports. Volume 8(2021)
• Page Start: 1599
• Page End: 1606
• Publication Date: 2021
• Subjects: Ach acetylcholine -- AhR aryl hydrocarbon receptor -- Ang II angiotensin II -- AT1 angiotensin II receptor type 1 -- BP systolic blood pressure -- eNOS endothelial nitric oxide synthase -- NO nitric oxide -- HCB hexachlorobenzene -- H&E hematoxylin and eosin -- PCBs polychlorinated biphenyls -- Phe phenylephrine -- POPs persistent organic pollutant -- SNP nitroprusside -- TGF-β1 Transforming Growth Factor-β1; Aorta -- AT1 -- Hexachlorobenzene -- Hypertension -- Losartan; Toxicology -- Periodicals; Clinical toxicology -- Periodicals; Drug-Related Side Effects and Adverse Reactions; Hazardous Substances; Poisoning; Toxicology; Electronic journals; Periodicals; Periodicals; 571.9505
• DOI: 10.1016/j.toxrep.2021.08.009
• Languages: English
• ISSNs: 2214-7500

Abstract

Graphical abstract: Highlights: Subchronic HCB-administration in male rats generates arterial hypertension. AT1 activity is involved in HCB- induced hypertension. AT1 activity is involved in arterial morphological changes caused by HCB. AT1 activity is involved in HCB- produced alterations in arterial relaxation. Losartan prevents HCB-produced alterations in TGF-β1, eNOS and AT1 expressions. Abstract: Environmental hexachlorobenzene (HCB) increases blood pressure (BP) in female rats, causing alterations in arterial structure and function. Here we study the role of Angiotensin II receptor type 1 (AT1) in HCB-induced hypertension through the use of AT1 antagonist losartan. HCB-treated male rats showed a 22.7% increase in BP which was prevented by losartan. Losartan blocked HCB-induced changes in arterial morphology (decreased aorta cell number and increased wall thickness). Losartan also prevented HCB-induced alterations in artery relaxation by acetylcholine and nitroprusside but not the reduction in the maximum contraction by phenylephrine. Losartan rescued arterial molecular alterations caused by HCB (i.e. an increase in TGF-β1 and AT1 expression and a decrease in eNOS expression and nitrite levels) and reduced hydrogen sulfide plasma concentration. In conclusion: in this work we demonstrate that AT1 activity is involved in HCB effects on the vascular system leading to hypertension.