Cardiac renin-angiotensin system (gene expression) and plasma angiotensin II in chickens with T3-induced pulmonary hypertension. Issue 4 (3rd July 2016)

• Record Type: Journal Article
• Authors: Hassanpour, H.; Afzali, A.; Fatemi Tabatabaie, R.; Torabi, M.; Alavi, Y.
• Is Part Of: British poultry science. Volume 57:Issue 4(2016)
• Page Start: 444
• Page End: 450
• Publication Date: 2016-07-03
• Subjects: Poultry -- Periodicals; Poultry industry -- Periodicals; 636.500941
• DOI: 10.1080/00071668.2016.1162284
• Languages: English
• ISSNs: 0007-1668

Abstract

Abstract: The relative expression of renin, angiotensin converting enzyme ( ACE ) and angiotensin II type 1 receptor ( AT1 R ) was performed using quantitative real-time PCR on tissue from the heart ventricles to investigate the effect of 3, 5, 3′-l-triiodothyronine (T3 )-induced pulmonary hypertension syndrome (PHS) in broiler chickens at 12 and 42 d of age. Plasma angiotensin II was also measured using enzyme immunoassay at 12, 21, 28, 32 and 42 d. Renin transcript in the right ventricle of the treated group was significantly increased at 12 d and decreased at 42 d of age compared to controls. ACE transcript in the left ventricle of the treated group was significantly increased at 42 d of age compared to controls. In the right ventricle, the expression of this gene was significantly increased at 12 d while decreased at 42 d of age in the treated group compared to control. AT1 R transcript in the right ventricle of the treated group was significantly increased at 12 and 42 d of age compared to control. In the left ventricle of the treated group, the transcript of this gene was only higher at 12 d of age than control. Plasma angiotensin II was significantly increased in pulmonary hypertensive chickens at 28 d of age compared to control. It is concluded that gene expression of renin, ACE and AT1 R was relatively upregulated in the heart of chickens developing pulmonary hypertension. The right ventricle of hearts from pulmonary hypertensive chickens showed considerable reductions of renin / ACE and elevation of AT1 R which may provide evidence of diminished responsiveness of the renin -angiotensin system.