Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats

Autor(es)

Zapparoli, Adriana ^[1] ; Figueiredo, Jose Francisco ^[1] ; Boer, Patricia Aline ^[1] ; Rocha Gontijo, Jose Antonio ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, Fac Ciencias Med, Lab Metab Hidrosalino Nucl Med & Cirurgia Expt, Disciplina Med Interna, Dept Clin Med, Ctr Med & Ci, BR-13083592 Campinas, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM; v. 12, n. 3, p. 161-168, SEP 2011.
• Citações Web of Science: 9

Resumo

The role of the central nervous system (CNS) in the control of blood pressure and hydrosaline homeostasis has been demonstrated by several studies. While circulating angiotensin II (AngII) tends to retain sodium by a direct renal action as well as through aldosterone release, stimulation of brain AngII receptors has been reported to induce natriuresis. Repetitive intracerebroventricular AngII injection was recently demonstrated to be capable of leading to desensitisation of the dipsogenic effect of AngII stimuli. The aim of the current study was to investigate a possible central desensitisation to AngII stimuli by observing the effects of a low-concentration solution of AngII on the dipsogenic and natriuretic mechanisms in conscious rats, compared with appropriate age-matched 0.15 M NaCl-injected subjects, as evaluated by lithium clearance. The present report confirmed earlier reports on the potent natriuretic and dipsogenic effects of central AngII receptor stimulation. Natriuresis is mediated by a decrease in sodium reabsorption in the proximal and post-proximal tubule segments of the nephron. The current findings lend further support to the idea that AngII, in the CNS, is instrumental in the regulation of body fluid homeostasis. The magnitude of the dipsogenic and renal response to AngII was significantly decreased by repetitive stimulus. (AU)

• Processo FAPESP: 06/52431-1 - Nefrogenese em um modelo genetico de hipertensao arterial primaria: implicacoes no desenvolvimento hipertensivo de ratos espontaneamente hipertensos (shr).
• Beneficiário: Jose Antonio Rocha Gontijo
• Modalidade de apoio: Auxílio à Pesquisa - Regular