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Titolo:
CALCIUM-CHANNEL ACTIVITY INCREASED BY PLASMA FROM ISCHEMIC HINDLIMBS OF RATS - ROLE OF AN ENDOGENOUS NO SYNTHASE INHIBITOR
Autore:
JIN JS; WILDE DW; WEBB RC; DALECY LG;
Indirizzi:
UNIV MICHIGAN,SCH MED,DEPT PHYSIOL,7799 MED SCI,BLDG 2,1301 E CATHERINE ST ANN ARBOR MI 48109 UNIV MICHIGAN,SCH MED,DEPT PHYSIOL ANN ARBOR MI 48109 UNIV MICHIGAN,SCH MED,DEPT ANESTHESIOL ANN ARBOR MI 48109 UNIV MICHIGAN,SCH MED,DEPT SURG ANN ARBOR MI 48109
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 4, volume: 39, anno: 1996,
pagine: 1484 - 1492
SICI:
0363-6135(1996)39:4<1484:CAIBPF>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; GENETIC-HYPERTENSION; BAY K-8644; CA-2+;
Keywords:
HYPERTENSION; PROTEIN KINASE C; AORTIC SURGERY; INTERMITTENT CLAUDICATION; VASCULAR SMOOTH MUSCLE; FURA-2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
J.S. Jin et al., "CALCIUM-CHANNEL ACTIVITY INCREASED BY PLASMA FROM ISCHEMIC HINDLIMBS OF RATS - ROLE OF AN ENDOGENOUS NO SYNTHASE INHIBITOR", American journal of physiology. Heart and circulatory physiology, 39(4), 1996, pp. 1484-1492

Abstract

We tested the hypothesis that an endogenous nitric oxide synthase (NOS) inhibitor released from ischemic hindlimbs increases the activity of calcium channels in vascular smooth muscle, thus contributing to theincreased contractile response to calcium agonists. Hindlimb ischemiawas generated in rats by infrarenal aortic cross clamping for 5 h, after which plasma was obtained from femoral vein blood. Incubating naive aortic rings (endothelium intact) for 2 h in plasma collected from ischemic rats significantly reduced relaxation to acetylcholine in precontracted rings and increased contraction to the calcium channel agonist, BAY K 8644. However, in isolated smooth muscle cells (without endothelium) loaded with fura-2, no difference was noted in BAY K 8644-stimulated intracellular calcium concentration. The contractile responsesto sodium fluoride, serotonin, and calcium ionophore A23187 were not different in either ischemic or control plasma-incubated rings. The augmentation of the contractile response to BAY K 8644 was significantlyinhibited by nitroglycerin (10(-8) M) and by exposure to calcium-freesolution. N-omega-nitro-L-arginine (without plasma incubation)-pretreated rings also demonstrated hyperresponsiveness to BAY K 8644. The increase in responsiveness to BAY K 8644 exhibited a negative correlation with the maximal relaxation to acetylcholine (r = -0.99), suggestingthat the apparent increase in activity of calcium channels is mediated through inhibition of nitric oxide by an endogenous NOS inhibitor onendothelium.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 21:22:58