Abstract
A flock of AA breed chickens were reared in peterstme brood-vait chamber and were provided with high energy pelleted feed. At 14 d of age, a total of 350 birds were randomly divided into 3 groups as follows: 100 birds were exposed to normal ambient temperature of 20°C for control group; 150 birds were exposed to lower ambient temperature of 11°C to induce ascites (treatment I); and another group of 100 birds were exposed to lower ambient temperature of 11°C and fed diet containing 1% L-arginine for ascitic prophylactic treatment (treatment II). Samples were collected from blood and abdominal fluid of chicken at 3, 4, 5, 6 and 7 wk of age subsequently, to analysis the contents of plasma endothelin (ET-1), angiotensin II (Ang II), cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP). The results indicated that the contents of cAMP, cGMP, and Ang II in treatment and ascitic broilers were higher than Ⅰ the corresponding control group (p<0.01, p<0.05), ET-1 of preascitic broilers were control group (p<0.05), while there was an insignificant difference with later ascitic broilers. The contents of cAMP and cGMP in treatment II were higher than the treatment I and control groups (p<0.01, p<0.05), whereas, the contents of Ang II were gradually decreased compared to the control group (p<0.05), the contents of ET-1 were insignificantly different. On further analysis, the increased plasma Ang II at low ambient temperature condition in broilers made endothelium cell secretion of increased ET-1, cAMP, cGMP and decreased NO. Therefore, low temperature accelerated ascites syndrome in broilers. Supplemently L-arginine can decrease ET-1, and increase cAMP and cGMP. It is concluded that cAMP mediated in broilers pulmonary hypertension syndrome. (Asian-Aust. J. Anim. Sci. 2004. Vol 17, No. 11 : 1570-1574)
Highlights
Cyclic guanosine monophosphate has been reported to antagonize the positive effects of cyclic adenosine monophosphate
Denninger et al (1999) demonstrated that physiologic levels of nitric oxide, which increases the production of Cyclic guanosine monophosphate (cGMP) via cyclic guanylate stimulation, does not exert a major regulatory effect on cardiac function in unstimulated cardiac muscle or myocytes. cyclic adenosine monophosphate (cAMP) induces iNOS
Commercial kit comes from Institute of RIA, PLA General hospital, China. Another plasma for angiotensin II (Ang II) assay was obtained from blood collected in ice-chilled tubes containing protase inhibitors, each sample was immediately centrifuged at 4°C and stored at -20°C
Summary
Cyclic guanosine monophosphate (cGMP) has been reported to antagonize the positive effects of cyclic adenosine monophosphate (cAMP). Current evidence indicates that circulating levels of ET, reflecting activation or inhibition of the ET axis, may, under certain conditions, have clinical diagnostic or prognostic importance and provide insight into the role of ET in the pathophysiology of a variety of cardiovascular and other disease processes. These include hypertension (Haak et al., 1992), congestive heart failure (Rodeheffer et al, 1992), and myocardial infarction etc. Angiotensin II can stimulate endothelin production, which has been shown to stimulate oxidative stress (Rajagopalan et al, 1996) This may potentiate the vasoconstrictor effect of Ang II. Experiments were carried out, to determine whether cAMP, cGMP, Ang II, and ET-1 functional or not during low ambient temperature condition and supplemented L-arginine in the diet for ascitic broiler
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