Cardiac renin-angiotensin system (gene expression) and plasma angiotensin II in chickens with T₃-induced pulmonary hypertension

Abstract

The relative expression of renin, angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) 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. AT1R 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 AT1R 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 AT1R which may provide evidence of diminished responsiveness of the renin-angiotensin system.

Changes in the expression of cardiac genes responsive to thyroid hormones in the chickens with cold-induced pulmonary hypertension

“…The amount of troponin I, ACTC1, MHCβ transcripts did not change in the present study during cold stress and PHS in the broilers with hypertrophic heart or congestive heart failure whereas in the mammals, the regulation of these genes was strongly influenced ( Kahaly and Dillmann, 2005 ). The reason for this controversy is not known but it could be regarding to species differences that in part, changes PHS pathogenesis in the birds as reported by previous studies ( Teshfam et al, 2006 ; Hassanpour et al, 2009 ; Hamal et al, 2010 ; Hassanpour et al, 2016a , b ).…”