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Titolo:
Altered potassium balance and aldosterone secretion in a mouse model of human congenital long QT syndrome
Autore:
Arrighi, I; Bloch-Faure, M; Grahammer, F; Bleich, M; Warth, R; Mengual, R; Drici, MD; Barhanin, J; Meneton, P;
Indirizzi:
INSERM, U367, F-75005 Paris, France INSERM Paris France F-75005INSERM, U367, F-75005 Paris, France CNRS, Inst Pharmacol Mol & Cellulaire, F-06560 Valbonne, France CNRS Valbonne France F-06560 Mol & Cellulaire, F-06560 Valbonne, France Univ Freiburg, Inst Physiol, D-79104 Freiburg, Germany Univ Freiburg Freiburg Germany D-79104 hysiol, D-79104 Freiburg, Germany CHU Nice, F-06000 Nice, France CHU Nice Nice France F-06000CHU Nice, F-06000 Nice, France
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 15, volume: 98, anno: 2001,
pagine: 8792 - 8797
SICI:
0027-8424(20010717)98:15<8792:APBAAS>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
TORSADE-DE-POINTES; K+ CHANNEL; GLOMERULOSA CELLS; BARTTERS-SYNDROME; HYPOKALEMIC ALKALOSIS; MEMBRANE-PROTEIN; LIDDLES-SYNDROME; ANGIOTENSIN-II; MUTATIONS; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Meneton, P INSERM, U367, 17 Rue Fer Moulin, F-75005 Paris, France INSERM 17 Rue Fer Moulin Paris France F-75005 05 Paris, France
Citazione:
I. Arrighi et al., "Altered potassium balance and aldosterone secretion in a mouse model of human congenital long QT syndrome", P NAS US, 98(15), 2001, pp. 8792-8797

Abstract

The voltage-dependent K+ channel responsible for the slowly activating delayed K+ current I-Ks is composed of pore-forming KCNQ1 and regulatory KCNE1subunits, which are mutated in familial forms of cardiac long QT syndrome. Because KCNQ1 and KCNE1 genes also are expressed in epithelial tissues, such as the kidneys and the intestine, we have investigated the adaptation ofKCNE1-deficient mice to different K+ and Na+ intakes, On a normal K+ diet,homozygous kcne1(-/-) mice exhibit signs of chronic volume depletion associated with fecal Na+ and K+ wasting and have lower plasma K+ concentration and higher levels of aldosterone than wild-type mice, Although plasma aldosterone can be suppressed by low K+ diets or stimulated by low Na+ diets, a high K+ diet provokes a tremendous increase of plasma aldosterone levels inkcne1(-/-) mice as compared with wild-type mice (7.1-fold vs. 1.8-fold) despite lower plasma K+ in kcne1(-/-) mice. This exacerbated aldosterone production in kcne1(-/-) mice is accompanied by an abnormally high plasma reninconcentration, which could partly explain the hyperaldosteronism. In addition, we found that KCNE1 and KCNQ1 mRNAs are expressed in the zona glomerulosa of adrenal glands where I-Ks may directly participate in the control ofaldosterone production by plasma K+, These results, which show that KCNE1 and I-Ks are involved in K+ homeostasis, might have important implications for patients with I-Ks-related long QT syndrome, because hypokalemia is a well known risk factor for the occurrence of torsades de pointes ventriculararrhythmia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 13:21:56