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Chronic Angiotensin II Infusion in Lewis Rats Does Not Reveal Sex Differences in Blood Pressure or Renal Injury Apparent in the mRen2.Lewis Strain
Author(s) -
Diz Holland,
Pendergrass Karl,
Westwood Brian,
Chappell Mark
Publication year - 2009
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.23.1_supplement.1013.3
Subject(s) - endocrinology , medicine , blood pressure , chemistry , angiotensin ii , creatinine , ovariectomized rat , proteinuria , kidney , renal cortex , estrogen
Sexual dimorphism in blood pressure is evident in hypertensive mRen(2).Lewis (mRen2), but not the normotensive Lewis rat. As circulating and renal angiotensin II (Ang II) levels are higher in male mRen2, we determined whether Ang II infusion (300 ng/kg/min, osmotic minipump, 2 wks) would also reveal sex differences in pressure and proteinuria in male (M) and female (F) Lewis rats, as well as in ovariectomized (OVX) females. Ang II infusion significantly elevated systolic blood pressure in all groups (157 + 4, n=18 M/F/OVX vs. 112 + 1 mm Hg, n=10 M/F); however, pressure was not different between groups. Proteinuria was also comparable between the male and female Lewis rats following Ang II (M: 3.5 + 0.6; F: 4.0 + 0.9 mg/mg creatinine), but was reduced in the OVX Lewis (0.7 + 0.2 mg/mg creatinine, p<0.05). Kidney angiotensin content was not different for Ang II or Ang‐(1‐7) in the renal cortex; however, medullary Ang II levels were lower in the OVX Lewis (OVX: 0.37 + 0.03; F: 0.66 + 0.16; M: 0.94 + 0.10 fmol/mg) while Ang‐(1‐7) content was higher in the female groups (OVX: 5.2 + 0.4; F: 5.3 + 0.3; M: 3.9 + 0.3 fmol/mg). In summary, chronic Ang II infusion in Lewis rats does not replicate the sex differences in pressure or proteinuria evident in the mRen2 strain. OVX increases blood pressure in the mRen2, but does not exacerbate pressure in female Lewis emphasizing key differences between models of Ang II infusion and genetic activation of the RAS.