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Titolo:
Ca2+ influx mediates enhanced alpha(2)-adrenergic contraction in aortas from rats treated with NOS inhibitor
Autore:
Mukundan, H; Kanagy, NL;
Indirizzi:
Univ New Mexico, Hlth Sci Ctr, Dept Cell Biol & Physiol, Vasc Physiol Grp,Albuquerque, NM 87131 USA Univ New Mexico Albuquerque NM USA 87131 ol Grp,Albuquerque, NM 87131 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 5, volume: 281, anno: 2001,
pagine: H2233 - H2240
SICI:
0363-6135(200111)281:5<H2233:CIMEAC>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; SPONTANEOUSLY HYPERTENSIVE RATS; NITRIC-OXIDE; ENDOTHELIAL DYSFUNCTION; MESENTERIC-ARTERY; CALCIUM CHANNELS; PROTEIN-KINASE; K+ CHANNELS; RECEPTORS; MEMBRANE;
Keywords:
N-omega-nitro-L-arginine; alpha(2)-adrenergic receptor; UK-14304; vascular smooth muscle cells; L-type voltage-dependent calcium channels; nifedipine; hypertension;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Mukundan, H Univ New Mexico, Hlth Sci Ctr, Dept Cell Biol & Physiol, Vasc Physiol Grp,915 Camino Salud NE, Albuquerque, NM 87131 USA Univ New Mexico 915 Camino Salud NE Albuquerque NM USA 87131 A
Citazione:
H. Mukundan e N.L. Kanagy, "Ca2+ influx mediates enhanced alpha(2)-adrenergic contraction in aortas from rats treated with NOS inhibitor", AM J P-HEAR, 281(5), 2001, pp. H2233-H2240

Abstract

Previously, we reported that aortic segments from rats made hypertensive with the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NNA) exhibit enhanced contractile sensitivity to both alpha (2)-adrenergic receptor (alpha (2)-AR) stimulation and to KCl-induced depolarization. We hypothesized that increased contractile responses to these agents was due to a change in the common effector L-type voltage-dependent calcium channel (VDCC). In aortic segments from control and L-NNA-treated rats, contraction to the alpha (2)-AR agonist UK-14304 stimulated Ca2+ influx but released intracellular Ca2+ only in control arteries. UK-14304-induced contraction was blocked by the VDCC antagonist nifedipine in both control and L-NNA aortas but contraction of aortas from L-NNA-treated rats was blocked by lower concentrations. Calcium imaging studies in fura 2-loaded freshly isolated aortic vascular smooth muscle cells also demonstrated UK-14304-stimulated Ca2+ influx sensitive to nifedipine only in cells from L-NNA-treated rats. We conclude that alpha (2)-AR contraction in the rat aorta is mediated primarily by Ca2 influx and that L-NNA-induced hypertension increases the dependence of this contraction on VDCCs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 16:23:20