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Titolo:
Insights into glucocorticoid-associated hypertension
Autore:
Brem, AS;
Indirizzi:
Rhode Isl Hosp, Div Pediat Nephrol, Providence, RI 02903 USA Rhode Isl Hosp Providence RI USA 02903 Nephrol, Providence, RI 02903 USA Brown Univ, Sch Med, Providence, RI 02912 USA Brown Univ Providence RI USA 02912 niv, Sch Med, Providence, RI 02912 USA
Titolo Testata:
AMERICAN JOURNAL OF KIDNEY DISEASES
fascicolo: 1, volume: 37, anno: 2001,
pagine: 1 - 10
SICI:
0272-6386(200101)37:1<1:IIGH>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; APPARENT MINERALOCORTICOID EXCESS; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2; CORTISOL-INDUCED HYPERTENSION; GLOMERULAR-FILTRATION RATE; COLLECTING DUCT CELLS; LOW-BIRTH-WEIGHT; ANGIOTENSIN-II; MESSENGER-RNA; BLOOD-PRESSURE;
Keywords:
hypertension; glucocorticoids; vascular smooth muscle; renal sodium transport; 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD);
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
100
Recensione:
Indirizzi per estratti:
Indirizzo: Brem, AS Rhode Isl Hosp, Div Pediat Nephrol, 593 Eddy St, Providence, RI 02903 USA Rhode Isl Hosp 593 Eddy St Providence RI USA 02903 , RI 02903 USA
Citazione:
A.S. Brem, "Insights into glucocorticoid-associated hypertension", AM J KIDNEY, 37(1), 2001, pp. 1-10

Abstract

The association between excess glucocorticoids and hypertension has been much discussed but poorly understood. From both clinical observations and laboratory studies, it is clear that glucocorticoids exert their effects at many different sites responsible for blood pressure regulation. Isoforms of the enzyme 11 beta -hydroxysteroid dehydrogenase (11 beta -HSD), located insteroid-responsive tissues, metabolize endogenously produced glucocorticoids, These enzymes limit steroid access to mineralocorticoid and/or glucocorticoid receptors. In the kidney, synthetic and endogenous glucocorticoids are capable of enhancing transepithelial sodium transport in the presence of11 beta -HSD inhibition. Proximal tubule reabsorption of sodium can be indirectly augmented after chronic exposure to glucocorticoids. In this segment, steroids have a permissive effect, increasing the expression of both Na+, K+ adenosine triphosphatase along the basolateral membrane and Na+-H+ exchanger along the apical membrane of epithetial cells. Although glucocorticoids themselves produce no increase in sodium reabsorption in this segment, angiotensin II-stimulated sodium transport is significantly greater in proximal tubular cells pretreated with glucocorticoids. The increased transportin distal renal segments is more direct and stems in part from glucocorticoid cross-over binding to mineralocorticoid receptors. In vascular tissue, synthetic and endogenous glucocorticoids, after inhibition of the dehydrogenase reaction, magnify the response to circulating vasoconstrictors, The effects of glucocorticoids in vascular tissue is indirect, upregulating the expression of receptors to many Vasoconstrictors and downregulating the effects of potential vasodilators. Thus, glucocorticoids have the potential to alter both circulating volume and Vascular resistance. (C) 2001 by the National Kidney Foundation, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/12/18 alle ore 00:21:34