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Titolo:
Increased Na+/H+ exchanger isoform 1 activity in spontaneously hypertensive rats: lack of mutations within the coding region of NHE1
Autore:
Orlov, SN; Adarichev, VA; Devlin, AM; Maximova, NV; Sun, YL; Tremblay, J; Dominiczak, AF; Postnov, YV; Hamet, P;
Indirizzi:
Univ Montreal, CHUM, Ctr Rech, Lab Pathophysiol Ion Transport Disorders, Montreal, PQ H2W 1T8, Canada Univ Montreal Montreal PQ Canada H2W 1T8 rs, Montreal, PQ H2W 1T8, Canada Univ Glasgow, Western Infirm, Dept Med & Therapeut, Glasgow G11 6NT, Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland G11 6NT ow G11 6NT, Lanark, Scotland Moscow State Univ, Lab Biomembranes, Moscow, Russia Moscow State Univ Moscow Russia Univ, Lab Biomembranes, Moscow, Russia Cardiol Res Ctr, Moscow 121552, Russia Cardiol Res Ctr Moscow Russia 121552 diol Res Ctr, Moscow 121552, Russia
Titolo Testata:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
fascicolo: 2, volume: 1500, anno: 2000,
pagine: 169 - 180
SICI:
0925-4439(20000221)1500:2<169:INEI1A>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; SODIUM-PROTON EXCHANGE; NA-H EXCHANGE; LITHIUM COUNTERTRANSPORT; INTRACELLULAR PH; CELLS; EXPRESSION; ANTIPORTER; PROTEINS; GENE;
Keywords:
Na+/H+ exchange; vascular smooth muscle; spontaneous hypertension;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Orlov, SN Univ Montreal, CHUM, Ctr Rech, Lab Pathophysiol Ion Transport Disorders, Campus Hotel Dieu,3850 Rue St Urbain, Montreal, PQ H2W 1T8, CanadaUniv Montreal Campus Hotel Dieu,3850 Rue St Urbain Montreal PQ Canada H2W 1T8
Citazione:
S.N. Orlov et al., "Increased Na+/H+ exchanger isoform 1 activity in spontaneously hypertensive rats: lack of mutations within the coding region of NHE1", BBA-MOL BAS, 1500(2), 2000, pp. 169-180

Abstract

Enhanced Na+/H+ exchange, measured as amiloride derivative-sensitive Na+ and H+ fluxes in cells with a preliminary acidified cytoplasm (Delta mu(H+)-induced Na+/H+ exchange), is one of the most prominent intermediate phenotypes of altered Vascular smooth muscle cell (VSMC) function in spontaneouslyhypertensive rats (SHR). Analysis of Na+/H+ exchange in F-2 hybrids of SHRand normotensive rats seems to be the most appropriate approach in the search for the genetic determinants of abnormal activity of this carrier. However, the measurement of Delta mu(H+)-induced Na+/H+ exchange is hardly appropriate for precise analysis of the carrier's activity in VSMC derived fromseveral hundred F-2 hybrids. To overcome this problem, we compared the rate of Na-22 influx under baseline conditions and in Na+-loaded (ouabain-treated) VSMC. The dose-dependency of the rate of Delta mu(H+)-induced H+ efflux as well as of Na-22 influx in control and ouabain-treated cells on ethylisopropylamiloride (EIPA) concentration were not different (K(0.5)similar to0.3 mu M), suggesting that these ion transport pathways are mediated by the same carrier. EIPA-sensitive Na-22 influx in Na+-loaded cells was similarto 6-fold higher than in ouabain-untreated VSMC and was increased by 50-70% in two different substrains of SHR. About the same increment of EIPA-sensitive Na-22 influx in Na+-loaded VSMC was observed in 5- to 6-week-old SHR (an age at which hypertension has not yet developed) as well as in stroke-prone SHR (SHRSP) with severe hypertension, indicating that the heightened activity of Na+/H+ exchange is not a consequence of long-term blood pressureelevation. To examine whether or not the augmented activity of Na+/H+ exchange in SHR is caused by mutation of NHE1, i.e. the only isoform of this carrier expressed in VSMC, we undertook single-stranded conformational polymorphism analysis of 23 NHE1 cDNA fragments from SHR and SHRSP and sequencingof the 456-2421 NHE1 cDNA fragment. This study did not reveal any mutationin the entire coding region of NHE1. The lack of mutation in the coding region of NHE1 indicates that the augmented activity of the ubiquitous Na+/Hexchanger in primary hypertension is caused by altered regulation of carrier turnover number or/and its plasma membrane content. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 14:50:23