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Titolo:
Brain renin-angiotensin system and sympathetic hyperactivity in rats aftermyocardial infarction
Autore:
Zhang, WG; Huang, BS; 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: 45, anno: 1999,
pagine: H1608 - H1615
SICI:
0363-6135(199905)45:5<H1608:BRSASH>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONGESTIVE-HEART-FAILURE; SPONTANEOUSLY HYPERTENSIVE RATS; BARORECEPTOR REFLEX; BLOOD-PRESSURE; NERVE ACTIVITY; VENTRICULAR-FUNCTION; BAROREFLEX CONTROL; OUABAIN; ANTAGONIST; ACTIVATION;
Keywords:
congestive heart failure; sympathetic nerve activity; arterial baroreflex; ouabain; guanabenz; stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Leenen, FHH UnivCanadaa, Inst Heart, Hypertens Unit, 40 Ruskin St, Ottawa,ON K1Y 4W7, Univ Ottawa 40 Ruskin St Ottawa ON Canada K1Y 4W7 ON K1Y 4W7,
Citazione:
W.G. Zhang et al., "Brain renin-angiotensin system and sympathetic hyperactivity in rats aftermyocardial infarction", AM J P-HEAR, 45(5), 1999, pp. H1608-H1615

Abstract

Blockade of brain "ouabain" prevents the sympathetic hyperactivity and impairment of baroreflex function in rats with congestive heart failure (CHF). Because brain "ouabain" may act by activating the brain renin-angiotensin system (RAS), the aim of the present study was to assess whether chronic treatment with the AT(1)-receptor blocker losartan given centrally normalizesthe sympathetic hyperactivity and impairment of baroreflex function in Wistar rats with CHF postmyocardial infarction (MI). After left coronary artery ligation (2 or 6 wk), rats received either intracerebroventricular losartan (1 mg . kg(-1) . day(-1), CHF-Los) or vehicle (CHF-Veh) by osmotic minipumps. To assess possible peripheral effects of intracerebroventricular losartan, one set of CHF rats received the same rate of losartan subcutaneously. Sham-operated rats served as control. After 2 wk of treatment, mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) at rest and in response to air-jet stress and intracerebroventricularinjection of the alpha(2)-adrenoceptor-agonist guanabenz were measured in conscious animals. Arterial baroreflex function was evaluated by ramp changes in MAP. Compared with sham groups, CHF-Veh groups showed impaired arterial baroreflex control of HR and RSNA, increased sympathoexcitatory and presser responses to air-jet stress, and increased sympathoinhibitory and hypotensive responses to guanabenz. The latter is consistent with decreased activity in sympathoinhibitory pathways. Chronic intracerebroventricular infusion of losartan largely normalized these abnormalities. In CHF rats, the same rate of infusion of losartan subcutaneously was ineffective. In sham-operated rats, losartan intracerebroventricularly or subcutaneously did not affect sympathetic activity. We conclude that the chronic increase in sympathoexcitation, decrease in sympathoinhibition, and desensitized baroreflex function in CHF all appear to depend on the brain RAS, since this whole pattern of changes can be normalized by chronic central AT(1)-receptor blockade with losartan.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 05:20:58