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Titolo:
Dysregulation of extracellular adenosine levels by vascular smooth muscle cells from spontaneously hypertensive rats
Autore:
Dubey, RK; Mi, Z; Gillespie, DG; Jackson, EK;
Indirizzi:
Univ Zurich Hosp, Frauenklin, Clin Endocrinol, Dept Obstet & Gynecol, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Pittsburgh, Med Ctr, Dept Med, Ctr Clin Pharmacol, Pittsburgh, PA USAUniv Pittsburgh Pittsburgh PA USA Ctr Clin Pharmacol, Pittsburgh, PA USA Univ Pittsburgh, Med Ctr, Dept Pharmacol, Pittsburgh, PA USA Univ Pittsburgh Pittsburgh PA USA tr, Dept Pharmacol, Pittsburgh, PA USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 2, volume: 21, anno: 2001,
pagine: 249 - 254
SICI:
1079-5642(200102)21:2<249:DOEALB>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIC-AMP; ANGIOTENSIN-II; BLOOD-PRESSURE; NITRIC-OXIDE; GROWTH; PATHWAY; INHIBITION; MODULATION; RECEPTORS; DEAMINASE;
Keywords:
adenosine deaminase; adenosine kinase; hypertension; proliferation; vascular disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Dubey, RK Univ Zurich Hosp, Frauenklin, Clin Endocrinol, Dept Obstet & Gynecol, D217,NORD-1, CH-8091 Zurich, Switzerland Univ Zurich Hosp D217,NORD-1Zurich Switzerland CH-8091 zerland
Citazione:
R.K. Dubey et al., "Dysregulation of extracellular adenosine levels by vascular smooth muscle cells from spontaneously hypertensive rats", ART THROM V, 21(2), 2001, pp. 249-254

Abstract

The objective of this investigation was to determine whether the regulation of extracellular adenosine levels by smooth muscle cells (SMCs) from conduit arteries (aorta) and resistance microvessels (renal arterioles) is different in spontaneously hypertensive rats (SHR) versus normotensive Wistar-Kyoto (WKY) rats. Basal extracellular adenosine levels were decreased in cultured aortic and arteriolar SHR SMCs, and the increase in extracellular adenosine levels induced by stimulation of the cAMP-adenosine pathway was lessin aortic and arteriolar SHR SMCs. Extracellular adenosine levels were lower in SHR SMCs, however, even when the cAMP-adenosine pathway was inhibitedwith 3-isobutyl-1-methylxanthine. Inhibition of adenosine kinase with iodotubercidin and inhibition of adenosine deaminase with erythro-9-(2-hydroxy-3-nonyl) adenine increased extracellular adenosine; however, only inhibition of adenosine deaminase equalized extracellular adenosine levels in SHR versus WKY SMCs. Membrane-disrupted SHR SMCs metabolized exogenous adenosine faster than WKY SMCs did, and this difference was abolished by inhibition of adenosine deaminase but not adenosine kinase. SHR SMCs demonstrated a greater proliferative response than WKY SMCs. This enhanced proliferative response was not blocked by adenosine per se or inhibition of adenosine kinase but was blocked by inhibition of adenosine deaminase and by 2-chloroadenosine (adenosine deaminase-resistant adenosine analogue). We conclude that dysregulation of extracellular adenosine levels exists in SHR SMCs, that this dysregulation is not due to a defect in the cAMP-adenosine pathway but rather to enhanced activity of adenosine deaminase, and that the dysregulation of extracellular adenosine mediates the enhanced proliferative response of SHR SMCs.

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Documento generato il 03/04/20 alle ore 07:56:43