Adrenal, kidney, and heart angiotensins in female murine Ren-2 transfected hypertensive rats.
We analyzed by high-performance liquid chromatography and radioimmunoassay angiotensin I (Ang I), Ang II, Ang-(1-7), and metabolites in the adrenal, kidney and heart of normotensive female Sprague-Dawley (SD) and transgenic hypertensive [TGR(mRen-2)27] rats carrying the murine Ren-2d renin gene. The monogenetic model of hypertensive rats had significant increases in adrenal Ang II; whereas in the kidney Ang II was unchanged, but Ang I and Ang-(1-7) were significantly lower. Cardiac Ang I, Ang II, and Ang-(2-10) were significantly reduced in transgenic rats, while Ang-(2-7) was increased. In SD and transgenic rats kidney and adrenal angiotensins increased primarily during estrus or proestrus. In female transgenic rats the increased adrenal Ang II and the sustained renal Ang II may contribute to the established phase of hypertension.
Senanayake
P S
PS
Eye Institute, The Cleveland Clinic Foundation, OH 44195, USA. senanap@cesmtp.ccf.org
Smeby
R R
RR
Martins
A S
AS
Moriguchi
A
A
Kumagai
H
H
Ganten
D
D
Brosnihan
K B
KB
D000311:Adrenal Glands / Q000378:metabolism*; D000803:Angiotensin I / Q000302:isolation & purification / Q000378:metabolism / Q000502:physiology; D000804:Angiotensin II / Q000302:isolation & purification / Q000378:metabolism / Q000502:physiology; D000809:Angiotensins / Q000097:blood / Q000302:isolation & purification* / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D030801:Animals, Genetically Modified; D002851:Chromatography, High Pressure Liquid; D004971:Estrus / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006973:Hypertension / Q000235:genetics; D007668:Kidney / Q000378:metabolism*; D051379:Mice; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000235:genetics; D019076:Transgenes
D000809:Angiotensins; D000804:Angiotensin II; D000803:Angiotensin I; D012083:Renin