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Titolo:
Nitric oxide inhibition of renal vasoconstrictor responses to sympathetic cotransmitters in the pig in vivo
Autore:
Malmstrom, RE; Bjorne, H; Alving, K; Weitzberg, E; Lundberg, JON;
Indirizzi:
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17177 acol, S-17177 Stockholm, Sweden Karolinska Hosp, Dept Anaesthesiol & Intens Care, S-17176 Stockholm, Sweden Karolinska Hosp Stockholm Sweden S-17176 Care, S-17176 Stockholm, Sweden
Titolo Testata:
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
fascicolo: 2, volume: 5, anno: 2001,
pagine: 98 - 104
SICI:
1089-8603(200104)5:2<98:NOIORV>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
RABBIT CAROTID-ARTERY; RAT TAIL ARTERY; L-ARGININE; RELAXING FACTOR; IN-VIVO; NERVE-STIMULATION; NEUROPEPTIDE-Y; CONTRACTILE RESPONSES; ENDOTHELIAL-CELLS; PULMONARY-ARTERY;
Keywords:
ATP; neuropeptide Y; nitric oxide; phenylephrine; sympathetic; vasoconstriction; in vivo;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Malmstrom, RE Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17177 Stockholm, Sweden
Citazione:
R.E. Malmstrom et al., "Nitric oxide inhibition of renal vasoconstrictor responses to sympathetic cotransmitters in the pig in vivo", NITRIC OXID, 5(2), 2001, pp. 98-104

Abstract

The object of the present study was to investigate the involvement of nitric oxide (NO) in the regulation of renal vasoconstrictor responses to sympathetic nerve activation, and each of the known sympathetic cotransmitters separately, in the pig in vice. Renal vasoconstrictor responses were elicited by sympathetic nerve stimulation, the alpha (1)-adrenoceptor agonist phenylephrine (10 nmol kg(-1), injected iv), neuropeptide Y (NPY, 120 pmol kg(-1), iv) acting on the NPY Y, receptor, and the stable ATP-analogue alpha,beta -methylene ATP (mATP, 10 nmol kg(-1)) presumably acting on the P2X(1) purinoceptor. Infusion of the NO-donor sodium nitroprusside, at a dose (0.1 mg kg(-1) h(-1), iv) that elevated renal blood flow (by 14 +/- 7%) and lowered mean arterial pressure (by 30 +/- 5%), inhibited renal vasoconstrictor responses to sympathetic nerve stimulation, phenylephrine, and NPY, but not to mATP. In contrast, injection of the NO synthase inhibitor N omega -nitro-L-arginine methyl ester, at a dose (10 mg kg(-1), iv) that lowered renal blood flow (by 47 +/- 4%) and elevated mean arterial pressure (by 28 +/- 8%), potentiated the renal vasoconstriction evoked by sympathetic nerve stimulation, phenylephrine, and NPY,but not mATP. It is concluded that endogenousNO may function as an inhibitory modulator of vasoconstrictor responses tothe sympathetic cotransmitters norepinephrine and NPY. In contrast, NO seems not to modify vasoconstrictor responses to the sympathetic cotransmitterATP, a discrepancy that may be due to differences in the types of receptors and intracellular effector mechanisms. (C) 2001 Academic Press.

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Documento generato il 01/04/20 alle ore 19:50:14