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Titolo:
Enhanced sympathoexcitatory and pressor responses to central Na+ in Dahl salt-sensitive vs. -resistant rats
Autore:
Huang, BS; Wang, H; Leenen, FHH;
Indirizzi:
Univ Ottawa, Inst Heart, Hypertens Unit, Ottawa, ON K1Y 4W7, Canada Univ Ottawa Ottawa ON Canada K1Y 4W7 ens Unit, Ottawa, ON K1Y 4W7, Canada
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 5, volume: 281, anno: 2001,
pagine: H1881 - H1889
SICI:
0363-6135(200111)281:5<H1881:ESAPRT>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; 11-BETA-HYDROXYSTEROID DEHYDROGENASE; SODIUM; OUABAIN; NERVE; AGE;
Keywords:
brain "ouabain"; cerebrospinal fluid sodium ion; hypertension; sympathoexcitation; guanabenz; air stress; baroreflex;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Leenen, FHH Univ Ottawa, Inst Heart, Hypertens Unit, 40 Ruskin St, Ottawa,ON K1Y 4W7,Canada Univ Ottawa 40 Ruskin St Ottawa ON Canada K1Y 4W7 Y 4W7,Canada
Citazione:
B.S. Huang et al., "Enhanced sympathoexcitatory and pressor responses to central Na+ in Dahl salt-sensitive vs. -resistant rats", AM J P-HEAR, 281(5), 2001, pp. H1881-H1889

Abstract

An enhanced responsiveness to increases in cerebrospinal fluid (CSF) Na+ by high salt intake may contribute to salt-sensitive hypertension in Dahl salt-sensitive (S) rats. To test this hypothesis, sympathetic and pressor responses to acute and chronic increases in CSF Na+ were evaluated. In conscious young (5-6 wk old) and adult (10-11 wk old) Dahl S and salt-resistant (R) rats as well as weight-matched Wistar rats, hemodynamic [blood pressure (BP) and heart rate (HR)] and sympathetic [renal sympathetic nerve activity (RSNA)] responses to 10-min intracerebroventricular infusions of artificialCSF (aCSF) and Na+-rich aCSF (containing 0.2-0.45 M Na+) were evaluated. Intracerebroventricular Na+-rich aCSF increased BP, RSNA, and HR in a dose-related manner. The extent of these increases was significantly larger in Dahl S versus Dahl R or Wistar rats and young versus adult Dahl S rats. In a second set of experiments, young Dahl S and R rats received a chronic intracerebroventricular infusion of aCSF or Na+-rich (0.8 M) aCSF (5 mul/h) for 14 days, with the use of osmotic minipumps. On day 14 in conscious rats, CSF was sampled and BP, HR, and RSNA were recorded at rest and in response toair stress, intracerebroventricular alpha (2)-adrenoceptor agonist guanabenz, intracerebroventricular ouabain, and intravenous phenylephrine and nitroprusside to estimate baroreflex function. The infusion of Na+ rich aCSF versus aCSF increased CSF Na+ concentration to the same extent but caused severe versus mild hypertension in Dahl S and Dahl R rats, respectively. Aftercentral Na+ loading, hypothalamus "ouabain" significantly increased in Dahl S and only tended to increase in Dahl R rats. Moreover, sympathoexcitatory and pressor responses to intracerebroventricular exogenous ouabain were attenuated by Na+-rich aCSF to a greater extent in Dahl S versus Dahl R rats. Responses to air-jet stress or intracerebroventricular guanabenz were enhanced by Na+-rich aCSF in both strains, but the extent of enhancement was significantly larger in Dahl S versus Dahl R. Na+-rich aCSF impaired arterial baroreflex control of RSNA more markedly in Dahl S versus R rats. These findings indicate that genetic control of mechanisms linking CSF Na+ with brain "ouabain" is altered in Dahl S rats toward sympathetic hyperactivity and hypertension.

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Documento generato il 26/09/20 alle ore 03:02:32