Ovariectomy is protective against renal injury in the high-salt-fed older mRen2. Lewis rat.
Studies in experimental animals and younger women suggest a protective role for estrogen; however, clinical trials may not substantiate this effect in older females. Therefore, the present study assessed the outcome of ovariectomy in older mRen2. Lewis rats subjected to a high-salt diet for 4 wk. Intact or ovariectomized (OVX, 15 wk of age) mRen2. Lewis rats were aged to 60 wk and then placed on a high-salt (HS, 8% sodium chloride) diet for 4 wk. Systolic blood pressures were similar between groups [OVX 169 +/- 6 vs. Intact 182 +/- 7 mmHg; P = 0.22] after the 4-wk diet; however, proteinuria [OVX 0.8 +/- 0.2 vs. Intact 11.5 +/- 2.6 mg/mg creatinine; P < 0.002, n = 6], renal interstitial fibrosis, glomerular sclerosis, and tubular casts were lower in OVX vs. Intact rats. Kidney injury molecule-1 mRNA, a marker of tubular damage, was 53% lower in the OVX HS group. Independent from blood pressure, OVX HS rats exhibited significantly lower cardiac (24%) and renal (32%) hypertrophy as well as lower C-reactive protein (28%). Circulating insulin-like growth factor-I (IGF-I) levels were not different between the Intact and OVX groups; however, renal cortical IGF-I mRNA and protein were attenuated in OVX rats [P < 0.05, n = 6]. We conclude that ovariectomy in the older female mRen2. Lewis rat conveys protection against salt-dependent increase in renal injury.
Yamaleyeva
Liliya M
LM
Hypertension & Vascular Research Center, Wake Forest University Health Sciences, Winston-Salem, NC 27157-1095, USA.
Pendergrass
Karl D
KD
Pirro
Nancy T
NT
Gallagher
Patricia E
PE
Groban
Leanne
L
Chappell
Mark C
MC
D000375:Aging / Q000378:metabolism; D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D020296:Animals, Congenic; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005355:Fibrosis; D006973:Hypertension / Q000150:complications* / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D006984:Hypertrophy; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D007668:Kidney / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D010052:Ovariectomy; D010446:Peptide Fragments / Q000378:metabolism; D011507:Proteinuria / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D012083:Renin / Q000235:genetics / Q000378:metabolism*; D012084:Renin-Angiotensin System; D017673:Sodium Chloride, Dietary
D000803:Angiotensin I; D000804:Angiotensin II; D002097:C-Reactive Protein; D015815:Cell Adhesion Molecules; D007334:Insulin-Like Growth Factor I; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D010446:Peptide Fragments; D012333:RNA, Messenger; D012083:Renin; D017673:Sodium Chloride, Dietary; C110936:Havcr1 protein, rat; C407223:NPHS2 protein; C473112:Ren2 protein, mouse; C113267:nephrin; C118790:angiotensin I (1-7)