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Titolo:
The cerebrovascular response to elevated potassium - role of nitric oxide in the in vitro model of isolated rat middle cerebral arteries
Autore:
Schuh-Hofer, S; Lobsien, E; Brodowsky, R; Vogt, J; Dreier, JP; Klee, R; Dirnagl, U; Lindauer, U;
Indirizzi:
Humboldt Univ, Charite Hosp, Dept Expt Neurol, D-10117 Berlin, Germany Humboldt Univ Berlin Germany D-10117 xpt Neurol, D-10117 Berlin, Germany
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 1-2, volume: 306, anno: 2001,
pagine: 61 - 64
SICI:
0304-3940(20010622)306:1-2<61:TCRTEP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
SOLUBLE GUANYLATE-CYCLASE; DEPENDENT PROTEIN-KINASE; EXTRACELLULAR POTASSIUM; SPREADING ISCHEMIA; SUBARACHNOID SPACE; SMOOTH-MUSCLE; CORTEX; ACTIVATION; INHIBITION; INCREASE;
Keywords:
nitric oxide; potassium; isolated rat middle cerebral artery; nitric oxide synthase-inhibition; modulatory role; guanosine-3 ',5 '-cyclic monophosphate; potassium channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Lindauer, U Humboldt Univ, Charite Hosp, Dept Expt Neurol, Schumannstr 20-21, D-10117 Berlin, Germany Humboldt Univ Schumannstr 20-21 Berlin GermanyD-10117 ermany
Citazione:
S. Schuh-Hofer et al., "The cerebrovascular response to elevated potassium - role of nitric oxide in the in vitro model of isolated rat middle cerebral arteries", NEUROSCI L, 306(1-2), 2001, pp. 61-64

Abstract

We investigated the role of nitric oxide (NO) in the vascular response to high extraluminal K+-concentrations in the in vitro model of isolated rat middle cerebral arteries (MCA). Under control conditions, rat MCA dilated at20, 30, 40 and 60 mM K+. At 80 mM K+, a slight vasoconstriction occurred. The unspecific NO synthase (NOS)-inhibitor L-omega-nitro-L-arginine (L-NNA)increased the resting tone at 3 mM K+ by 31 +/- 5% (P < 0.01). While the vasodilatative effect of 20 mM K+ was unaffected by L-NNA, NOS-inhibition resulted in vasoconstriction at <greater than or equal to> 40 mM K+ (P < 0.01). In presence of L-NNA, the basal vessel diameter was restored by either the NO-donor S-nitroso-N-acetylpenicillamine (SNAP) or the cell-permeable guanosine-3',5'-cyclic monophosphate (cGMP) analogue 8-Br-cGMP. Co-application of L-NNA with either SNAP or 8-Br-cGMP resulted in partial restitution ofthe vasodilatative effect of 40 mM K+, respectively. In presence of the soluble guanylyl cyclase inhibitor 1 H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), the vascular response to 40 mM K+ was abolished. Our findings together with findings from the literature indicate a modulator role of NO at K+ <greater than or equal to> 40 mM K+, involving a cGMP-dependent mechanism. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 20:25:34