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Titolo:
BRAIN OUABAIN, ANG-II, AND SYMPATHOEXCITATION BY CHRONIC CENTRAL SODIUM LOADING IN RATS
Autore:
HUANG BS; VEERASINGHAM SJ; LEENEN FHH;
Indirizzi:
UNIV OTTAWA,INST HEART,DIV CARDIOL,HYPERTENS UNIT H360,1053 CARLING AVE OTTAWA ON K1Y 4E9 CANADA UNIV OTTAWA,INST HEART,DIV CARDIOL,HYPERTENS UNIT H360 OTTAWA ON K1Y 4E9 CANADA
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 4, volume: 43, anno: 1998,
pagine: 1269 - 1276
SICI:
0363-6135(1998)43:4<1269:BOAASB>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; SALT-SENSITIVE RATS; CHRONIC CEREBROVENTRICULAR INFUSION; ELEVATES BLOOD-PRESSURE; SYMPATHETIC HYPERACTIVITY; BARORECEPTOR REFLEX; ARTERIAL BAROREFLEX; ANGIOTENSIN-II; ATTENUATION; RESPONSES;
Keywords:
CEREBROSPINAL FLUID SODIUM; BAROREFLEX; SYMPATHETIC NERVE ACTIVITY; GUANABENZ;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
B.S. Huang et al., "BRAIN OUABAIN, ANG-II, AND SYMPATHOEXCITATION BY CHRONIC CENTRAL SODIUM LOADING IN RATS", American journal of physiology. Heart and circulatory physiology, 43(4), 1998, pp. 1269-1276

Abstract

Both brain ouabain-like activity (''ouabain'') and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and presser responsesto high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. To assess whether increases in cerebrospinal fluid (CSF) sodium can mimic this pattern of changes, Wistar rats were chronically infused with artificial CSF (aCSF) or sodium-rich aCSF(0.8 or 1.2 M sodium) intracerebroventricularly through osmotic minipumps for 14 days. Sodium-rich aCSF (0.8 M) was also infused intracerebroventricularly for 2 wk concomitantly with either antibody Fab fragments that bind ouabain and related steroids with high affinity, gamma-globulins as control (200 mu g/day for both), or the AT(1) blocker losartan (1 mg.kg(-1).day(-1)). Sodium-rich aCSF increased CSF sodium from146 +/- 2 to 152 +/- 2 (0.8 M) and 160 +/- 3 (1.2 M) mmol/l, and increased brain ''ouabain'' in the hypothalamus, pituitary, and pens. In conscious rats, sodium-rich aCSF increased baseline mean arterial pressure (MAP), enhanced MAP, heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular alpha(2)-adrenoceptor agonist guanabenz and air stress, and desensitized arterial and cardiopulmonary baroreflex control of HR and RSNA. These effects were largely prevented by intracerebroventricular Fab fragments or losartan. Thus, in Wistar rats, both brain ''ouabain'' and the brain renin-angiotensin system contribute to sympathoexcitation, impairment of baroreflexes, and hypertension caused by chronically increased CSF sodium. The similar patterns of changes caused by CSF sodium in Wistar rats and by high sodium intake in SHR and Dahl S rats indicate that if high sodium intake increases central sodium, such changes may contribute to sympathoexcitation and hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 06:08:30