Chronic restraint stress increases angiotensin II potency in the rat carotid: role of cyclooxygenases and reactive oxygen species

• Published in: Journal of pharmacy and pharmacology Vol. 69; no. 1; p. 52
• Main Authors: Côco, Hariane, Pernomian, Larissa, Pereira, Priscila C, Gomes, Mayara S, Marchi, Katia C, Lopes, Alexandre H, Cunha, Thiago M, Tirapelli, Carlos R, de Oliveira, Ana M
• Format: Journal Article
• Language: English
• Published: England 01.01.2017
• Subjects: 6-Ketoprostaglandin F1 alpha - metabolism; Angiotensin II - metabolism; Animals; Carotid Arteries - metabolism; Catalase - metabolism; Corticosterone - blood; Cyclooxygenase 1 - metabolism; Cyclooxygenase 2 - metabolism; Cyclooxygenase Inhibitors; Endothelium, Vascular - metabolism; Hydrogen Peroxide - metabolism; Male; Muscle Contraction; Muscle, Smooth, Vascular - physiology; NADPH Oxidase 4; NADPH Oxidases - metabolism; Oxadiazoles - metabolism; Phosphatidylinositol 3-Kinases - metabolism; Prostaglandin-Endoperoxide Synthases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Rats, Wistar; Reactive Oxygen Species - metabolism; Restraint, Physical; Stress, Psychological - etiology; Stress, Psychological - metabolism; Stress, Psychological - physiopathology; Vasoconstriction; chronic restraint stress; Akt; prostacyclin; angiotensin II; hydrogen peroxide
• ISSN: 2042-7158
• DOI: 10.1111/jphp.12659

To investigate the mechanisms underlying the effects of chronic restraint stress on the vascular contractile response induced by angiotensin (Ang) II in rat carotid. Concentration-response curves for AngII were obtained in endothelium-intact or endothelium-denuded carotid rings, in the absence or presence of SC-560 (COX-1 inhibitor), SC-236 (COX-2 inhibitor), wortmannin (PI K-Akt inhibitor), ML171 (NOX-1 inhibitor), VAS2870 (NOX-4 inhibitor), tiron (O2- scavenger) or PEG-catalase (H O scavenger). 6-ketoPGF , TXB , O2- or H O levels and superoxide dismutase and catalase activity or expression were also measured in rat carotid. Stress increased AngII potency in rat carotid. Muscular COX-1 or COX-2-derived metabolites negatively modulated AngII-induced contraction in control rat carotid. Endothelial COX-1 or COX-2-derived metabolites positively modulated AngII-induced contraction in stressed rat carotid. PI K-Akt, NOX-1, NOX-4, O2- and H O positively modulated AngII-induced contraction in stressed rat carotid. Stress increased 6-ketoPGF or H O generation and reduced catalase activity in rat carotid. Protein expression of COX-1, NOX-4 or p-Akt was increased in stressed rat carotid. Stress increases AngII potency in rat carotid by a mechanism that involves the increased generation of PGI and H O and the activation of Akt pathway. Such mechanism could play a pathophysiological role in cardiovascular diseases correlated with stress.