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Titolo:
Role of nitric oxide in modulating renal function and arterial pressure during chronic aldosterone excess
Autore:
Granger, JP; Kassab, S; Novak, J; Reckelhoff, JF; Tucker, B; Miller, MT;
Indirizzi:
Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA Univ Mississippi Jackson MS USA 39216 ol & Biophys, Jackson, MS 39216 USA Univ Mississippi, Med Ctr, Ctr Excellence Cardiovasc Renal Res, Jackson, MS Univ Mississippi Jackson MS USA 39216 e Cardiovasc Renal Res, Jackson, MS
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 1, volume: 45, anno: 1999,
pagine: R197 - R202
SICI:
0363-6119(199901)45:1<R197:RONOIM>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-II; ESCAPE; HYPERTENSION; SALT; NATRIURESIS; INHIBITION; SYSTEMS; DOGS;
Keywords:
endothelium; kidney; hypertension;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Granger, JP Univ,Mississippi, Med Ctr, Dept Physiol & Biophys, 2500 N State St, Jackson Univ Mississippi 2500 N State St Jackson MS USA 39216 Jackson
Citazione:
J.P. Granger et al., "Role of nitric oxide in modulating renal function and arterial pressure during chronic aldosterone excess", AM J P-REG, 45(1), 1999, pp. R197-R202

Abstract

Chronic aldosterone (Aldo) excess is associated with transient sodium retention, extracellular fluid volume expansion, renal vasodilation, and hypertension. The purpose of this study was to determine the role of nitric oxide(NO) in mediating the renal vasodilation and the escape from the sodium-retaining actions of Aldo. To achieve this goal, we examined the long-term effects of Aldo (15 mu g.kg(-1).min(-1) for 7 days) in conscious, chronicallyinstrumented control dogs (n = 9) and in dogs (n = 12) pretreated with theNO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mu g.kg(-1).min(-1)). In control dogs, Aldo caused a transient sodium retention (126 +/- 6 to 56 +/- 2 meq/day) followed by a return of sodium excretion to normal levels. Aldo also increased renal plasma flow by 15% (205 +/- 13 to 233 +/- 16 ml/min), glomerular filtration rate by 20% (72 +/- 3 to 87 +/- 5ml/min), and arterial pressure from 90 +/- 3 to 102 +/- 3 mmHg. Aldo increased urinary nitrate/nitrite excretion by 60% in the control dogs. Althoughthe sodium-retaining (144 +/- 7 to 56 +/- 7 meq/day) and arterial pressure(122 +/- 6 to 136 +/- 5 mmHg) responses to Aldo were the same in dogs pretreated with L-NAME compared with control, the renal hemodynamic response was markedly attenuated. The results of this study suggest that NO plays an important role in mediating the renal vasodilation during chronic Aldo excess.

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Documento generato il 28/11/20 alle ore 04:52:04