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Angiotensin II and developmental cardiovascular‐renal interactions in embryonic chickens
Author(s) -
Mueller Casey A,
Crossley Dane A,
Burggren Warren W
Publication year - 2013
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.27.1_supplement.714.18
Subject(s) - captopril , endocrinology , medicine , angiotensin ii , renin–angiotensin system , angiotensin converting enzyme , embryo , blood pressure , kidney , saline , mean arterial pressure , biology , incubation , chemistry , heart rate , biochemistry , microbiology and biotechnology
The role of Angiotensin II (ANGII) in cardiovascular‐renal interactions during embryonic development of White Leghorn chickens ( Gallus gallus domesticus ) was examined. Captopril, an angiotensin‐converting enzyme (ACE) inhibitor, or control saline, was delivered via the egg air cell on days 5–18. Masses, fluid osmolality and mean arterial pressure (MAP) and heart rate ( f H ) were measured on day 19 (90% of incubation). Embryo and heart masses did not differ between control and captopril embryos, but kidney wet and dry masses were both 10% larger in captopril embryos. In addition, blood osmolality was significantly lower. Captopril embryos were significantly hypotensive, with a MAP 15% lower than controls, but f H did not differ. MAP and f H of captopril embryos did not respond to an injection of Angiotensin I (ANGI), confirming ACE inhibition. ANGII induced a stronger hypertensive response in captopril embryos, with adrenergic and ganglionic blockade indicating that this was due to peripheral catecholamines. Chronic removal of embryonic ANGII has both cardiovascular and renal effects, implying “crosstalk” between the developing systems. Funding from NSF (IOS‐1025823) to WB.