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Titolo:
RENAL VASCULAR INDUCTION OF TGF-BETA-2 AND RENIN BY POTASSIUM-DEPLETION
Autore:
RAY PE; MCCUNE BK; GOMEZ RA; HORIKOSHI S; KOPP JB; KLOTMAN PE;
Indirizzi:
NIDR,DEV BIOL LAB BETHESDA MD 20892 UNIV VIRGINIA,MED CTR,SCH MED,DEPT NEPHROL CHARLOTTESVILLE VA 22901 CHILDRENS NATL MED CTR,CHILDRENS RES INST WASHINGTON DC 00000 JOHNS HOPKINS & FRANCIS SCOTT KEY MED CTR,DEPT PATHOL BALTIMORE MD 00000
Titolo Testata:
Kidney international
fascicolo: 5, volume: 44, anno: 1993,
pagine: 1006 - 1013
SICI:
0085-2538(1993)44:5<1006:RVIOTA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSFORMING GROWTH FACTOR-BETA-1; SMOOTH-MUSCLE CELLS; ANGIOTENSINOGEN GENE-EXPRESSION; FACTOR TGF-BETA; RAT-KIDNEY; PROLIFERATION; SECRETION; HYPERPLASIA; HYPERTROPHY; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
P.E. Ray et al., "RENAL VASCULAR INDUCTION OF TGF-BETA-2 AND RENIN BY POTASSIUM-DEPLETION", Kidney international, 44(5), 1993, pp. 1006-1013

Abstract

Recently, we have found that transforming growth factor (TGF)-beta2 and renin are abundantly expressed in the juxtaglomerular apparatus (JGA) of dehydrated mice. Since potassium (K+) depletion also stimulates renin and induces hypertrophy of the JGA, we examined the ability of this maneuver to stimulate TGF-beta isoforms and renin in renovascular tissue and the JGA of young rats. Sprague-Dawley rats (50 +/- 5 g) were fed either a control diet or a potassium-deficient diet (< 0.05% K) for 7, 16, or 21 days. As a control for TGF-beta and renin stimulation, an additional group of animals was fed a normal diet but was water deprived for three days. Potassium-depleted animals experienced severe growth retardation but kidney weight increased significantly. Potassium depletion induced both TGF-beta2 and renin immunoreactivity in renalarterioles and the JGA but had no effect on TGF-beta1 and TGF-beta3 isoforms. To determine the role of circulating angiotensin II in the stimulation of TGF-beta2 by potassium depletion, a group of potassium-depleted rats received enalapril (100 mg/liter) in the drinking water. The addition of converting enzyme inhibitor increased both the intensity of TGF-beta2 and renin staining as well as the number of cells positively stained. Our results demonstrate that K+ depletion induces TGF-beta2 and renin in renal arterioles and in the JGA. Furthermore, circulating angiotensin II is not responsible for the increase in the local expression of TGF-beta2. These findings suggest that TGF-beta2 may be an important mediator of JGA hypertrophy. The simultaneous induction of TGF-beta2 with renin suggests that these factors may be coregulated.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 11:20:48