Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Pressure-independent contribution of sodium to large artery structure and function in hypertension
Autore:
Safar, ME; Thuilliez, C; Richard, V; Benetos, A;
Indirizzi:
Broussais Hosp, Dept Internal Med, Paris, France Broussais Hosp Paris France sais Hosp, Dept Internal Med, Paris, France Broussais Hosp, INSERM U337, Paris, France Broussais Hosp Paris FranceBroussais Hosp, INSERM U337, Paris, France Pharm Rouen, Fac Med, F-76183 Rouen, France Pharm Rouen Rouen France F-76183 m Rouen, Fac Med, F-76183 Rouen, France
Titolo Testata:
CARDIOVASCULAR RESEARCH
fascicolo: 2, volume: 46, anno: 2000,
pagine: 269 - 276
SICI:
0008-6363(200005)46:2<269:PCOSTL>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONVERTING-ENZYME-INHIBITION; RECEPTOR GENE POLYMORPHISM; OXIDE SYNTHASE GENE; ANGIOTENSIN-II; MECHANICAL-PROPERTIES; CAROTID-ARTERY; AORTIC STIFFNESS; WALL PROPERTIES; BLOOD-PRESSURE; RATS;
Keywords:
arteries; diuretic agents; extracellular matrix; hypertension; water electrolyte balance;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Safar, ME Broussais Hosp, Dept Internal Med, Paris, France Broussais HospParis France Dept Internal Med, Paris, France
Citazione:
M.E. Safar et al., "Pressure-independent contribution of sodium to large artery structure and function in hypertension", CARDIO RES, 46(2), 2000, pp. 269-276

Abstract

Background: Sodium sensitivity is usually studied in terms of change of blood pressure (BP) but the specific effects on conduit arteries have not been addressed. Experimental studies: In genetic models of hypertension. chronically increased sodium diet is associated with aortic hypertrophy and development of extracellular matrix independent of BP. These alterations, oftenassociated with increased stiffness and secretory properties of vascular smooth muscle, are reversed by lowering sodium intake and/or giving diuretics, independently of BP changes. The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodiumintake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade. Clinical studies: In longitudinal studies on hypertensive subjects, increased sodium intake not only increases BP but also decreases brachial artery diameter, implying pressure-independent mechanisms acting on the arterial wall. The antihypertensive effect of diuretics is associated with little change of arterial geometry and stiffness, probably resulting frommarked angiotensin-induced increase of arterial stiffness. This latter effect is blocked by converting-enzyme inhibition. All these arterial changes may be genetically modulated since in salt-sensitive hypertensives, increased sodium intake is associated with decreased arterial distensibility, and in some hypertensive subjects, a polymorphism of the AT(1)-receptor gene has been described in association with increased aortic stiffness and is reversed by converting-enzyme inhibition independent of BP. Conclusion: In genetic models of human and rat hypertension, increased sodium intake is associated with specific alterations of the structure and function of conduit arteries involving extracellular matrix, but independent of BP and atherosclerosis. (C) 2000 Elsevier Science BN. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 00:05:36