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Hypoxic incubation alters cardiovascular response to Ang II in embryonic chickens ( Gallus gallus ) (1067.3)
Author(s) -
Tate Kevin,
Crossley Dane
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1067.3
Subject(s) - endocrinology , medicine , incubation , angiotensin ii , renin–angiotensin system , blockade , receptor , hypoxia (environmental) , pressor response , homeostasis , embryogenesis , adrenergic receptor , biology , blood pressure , embryo , chemistry , heart rate , microbiology and biotechnology , oxygen , biochemistry , organic chemistry
The renin angiotensin system (RAS) is a critical regulatory mechanism contributing to cardiovascular homeostasis. Angiotensin II (Ang II) is the primary peptide of the system eliciting a strong vasopressor response. While blood volume stress has been the primary perturbation used to study the RAS during vertebrate development, hypoxia has been largely ignored. We hypothesized that the RAS activity would increase and the pressor response to Ang II would be attenuated in embryonic chickens subjected to chronic hypoxic (15% O2) stress. We investigated some of the components that underlie the Ang II cardiovascular response in chicken embryos and how 15% O2 incubation alters the response. Hypoxic incubation blunted the pressor response to Ang I, and Ang II in embryonic chickens. Following alpha‐adrenergic receptor blockade, the pressor response to Ang II was blunted in the normoxic but not the hypoxic embryos. In addition following alpha‐adrenergic blockade the Ang II pressure response did not differ between the normoxic and hypoxic incubated embryos. This suggests that hypoxic incubation blunts the pressor response to Ang II possibly attributed to saturation of the alpha‐adrenergic receptors in embryonic chickens. Grant Funding Source : Supported by NSF career grant to DAC IBN IOS 084574