Captopril modulates vasoactive and oxidative pathways in broiler chickens exposed to high-altitude and cold stress.

Abstract

High-altitude hypoxia and cold stress challenge broiler production by inducing oxidative stress and vasoactive imbalances, primarily through activation of the renin-angiotensin system (RAS). This study investigated whether dietary captopril, an ACE inhibitor, could mitigate these adverse effects. 240 one-day-old broilers were randomly assigned to four diets: a basal control diet or the basal diet supplemented with 10 (CAP10), 20 (CAP20), or 30 (CAP30) mg captopril/kg feed. Birds were reared at 2100 m altitude under cold stress. Growth performance, carcass characteristics, ascites-related mortality, pulmonary hypertension syndrome (PHS) index (right ventricle to total ventricle ratio; RV:TV), blood parameters [angiotensin-converting enzyme (ACE), nitric oxide (NO), malondialdehyde (MDA), heterophil-to-lymphocyte ratio (H:L)], and pulmonary gene expression [endothelial and inducible nitric oxide synthases (eNOS, iNOS), endothelin-1 (ET1), superoxide dismutase-1 (SOD1), and glutathione peroxidase (GPX)] were evaluated. CAP20 and CAP30 groups showed improved feed conversion ratio during the finisher phase. They also exhibited higher carcass, breast, and thigh yields, and reduced heart weight, RV:TV ratio, and ascites mortality. Biochemically, these groups had significantly lower ACE activity and MDA levels, and higher NO levels. The H:L ratio decreased in all captopril groups. Gene expression analysis revealed upregulated eNOS, iNOS, SOD1, and GPX, and downregulated ET1 in the CAP20 and CAP30 groups. It is concluded that dietary captopril at 20-30 mg/kg effectively ameliorates high-altitude and cold stress in broilers by inhibiting ACE, thereby improving vascular function, enhancing antioxidant defenses, reducing oxidative stress and inflammation, and ultimately improving production performance and cardiopulmonary health.