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Titolo:
Expression of angiotensinogen mRNA and protein in angiotensin II-dependenthypertension
Autore:
Kobori, H; Harrison-Bernard, LM; Navar, LG;
Indirizzi:
Tulane Univ, Sch Med, Dept Physiol, New Orleans, LA 70112 USA Tulane UnivNew Orleans LA USA 70112 t Physiol, New Orleans, LA 70112 USA
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 3, volume: 12, anno: 2001,
pagine: 431 - 439
SICI:
1046-6673(200103)12:3<431:EOAMAP>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOLECULAR-WEIGHT ANGIOTENSINOGEN; RECEPTOR MESSENGER-RNA; RAT PROXIMAL TUBULE; INFUSED RATS; IMMUNOCYTOCHEMICAL LOCALIZATION; BLOOD-PRESSURE; AT(1) RECEPTOR; PREGNANT-WOMEN; CELL-LINE; KIDNEY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Kobori, H Tulane Univ, Sch Med, Dept Physiol, 1430 Tulane Ave,SL39, New Orleans, LA 70112 USA Tulane Univ 1430 Tulane Ave,SL39 New Orleans LA USA 70112 12 USA
Citazione:
H. Kobori et al., "Expression of angiotensinogen mRNA and protein in angiotensin II-dependenthypertension", J AM S NEPH, 12(3), 2001, pp. 431-439

Abstract

Chronic elevations in circulating angiotensin II (AngII) levels produce sustained hypertension and increased intrarenal AngII contents through multiple mechanisms, which may include sustained or increased local production ofAngII. This study was designed to test the hypothesis that chronic AngII infusion increases renal angiotensinogen mRNA and protein levels, thus contributing to the increase in intrarenal AngII levels. AngII (80 ng/min) was infused subcutaneously for 13 d into Sprague-Dawley rats, using osmotic minipumps. Control rats underwent sham operations. By day 12, systolic arterialBP increased to 184 +/- 3 mmHg in AngII-treated rats, whereas values for sham-treated rats remained at control levels (125 +/- 1 mmHg). Plasma renin activity was markedly suppressed (0.2 +/- 0.1 versus 5.3 +/- 1.2 ng AngI/mlper h); however, renal AngII contents were significantly increased in AngII-treated rats (273 +/- 29 versus 99 +/- 18 fmol/g). Western blot analyses of plasma and liver protein using a polyclonal anti-angiotensinogen antibody demonstrated two specific im munoreactive bands, at 52 and 64 kD, whereaskidney tissue exhibited one band, at 52 kD. Densitometric analyses demonstrated that AngII infusion did not alter plasma (52- or 64-kD), renal (52-kD), or hepatic (52-kD) angiotensinogen protein levels; however, there was a significant increase in hepatic expression of the highly glycosylated 64-kDangiotensinogen protein, of almost fourfold (densitometric value/control value ratios of 3.79 +/- 1.16 versus 1.00 +/- 0.35). Renal and hepatic expression of angiotensinogen mRNA, which was examined by semiquantitative reverse transcription-PCR, was significantly increased in AngII-treated rats, compared with sham-treated rats (kidney, densitometric value/glyceraldehyde-3-phosphate dehydrogenase mRNA value ratios of 0.82 +/- 0.11 versus 0.58 +/-0.04; liver, densitometric value/glyceraldehyde-3-phosphate dehydrogenase mRNA value ratios of 2.34 +/- 0.07 versus 1.32 +/- 0.15). These results indicate that increases in circulating AngII levels increase intrarenal angiotensinogen mRNA levels, which may contribute to the sustained renal AngII-generating capacity that paradoxically occurs in AngII-treated hypertensive rats.

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Documento generato il 22/01/20 alle ore 09:28:42