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

Autor: Susana Gorzalczany, Zahira Deza, Giselle Romero Caimi, Rocío Castilla, María Inés Rosón, Laura Alvarez, Patricia Bonazzola
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Ach
acetylcholine
medicine.medical_specialty
Health
Toxicology and Mutagenesis
Toxicology
Losartan
AT1
BP
systolic blood pressure
Enos
PCBs
polychlorinated biphenyls
Internal medicine
medicine.artery
RA1190-1270
medicine
Hexachlorobenzene
SNP
nitroprusside
Receptor
Phenylephrine
Aorta
ComputingMethodologies_COMPUTERGRAPHICS
TGF-β1
Transforming Growth Factor-β1
Ang II
angiotensin II
NO
nitric oxide
Angiotensin II receptor type 1
biology
Chemistry
HCB
hexachlorobenzene
eNOS
endothelial nitric oxide synthase
Regular Article
POPs
persistent organic pollutant
biology.organism_classification
Angiotensin II
Phe
phenylephrine
Blood pressure
Endocrinology
AhR
aryl hydrocarbon receptor
Toxicology. Poisons
Hypertension
cardiovascular system
H&E
hematoxylin and eosin
hormones
hormone substitutes
and hormone antagonists
AT1
angiotensin II receptor type 1
medicine.drug
circulatory and respiratory physiology
Zdroj: Toxicology Reports
Toxicology Reports, Vol 8, Iss, Pp 1599-1606 (2021)
ISSN: 2214-7500
Popis: 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.
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.
Databáze: OpenAIRE
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