Effects of acute AV3V lesions on renal and hindlimb vasodilation induced by volume expansion

Effects of acute AV3V lesions on renal and hindlimb vasodilation induced by volume expansion

Author Colombari, Debora Simões de Almeida Autor UNIFESP Google Scholar
Cravo, Sergio Luiz Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Abstract The role of the anteroventral third ventricle (AV3V) region in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (1% body weight, 1.4 mL/min) was studied in urethane-anesthetized rats. In sham-lesioned animals, VE produced a transitory (less than or equal to 20 minutes) increase in mean arterial pressure, which peaked at 10 minutes (10+/-3 mm Hg), and sustained increases of renal (123+/-10% and 127+/-6% of baseline, respectively, 10 and 40 minutes after VE) and hindlimb vascular (157+/-19% and 153+/-9% of baseline) conductance. After AV3V lesions, VE induced a sustained increase in mean arterial pressure. Although renal blood flow increased in response to VE, renal vascular conductance was unaffected, indicating that renal vasodilation was abolished. On the other hand, after AV3V lesions, the increases in hindlimb blood flow and vascular conductance were higher than those observed in sham-lesioned rats. Results obtained demonstrated that the AV3V region is essential for the renal vasodilation induced by VE.
Keywords blood flow velocity
brain
rats
blood pressure
water-electrolyte balance
Language English
Date 1999-10-01
Published in Hypertension. Philadelphia: Lippincott Williams & Wilkins, v. 34, n. 4, p. 762-767, 1999.
ISSN 0194-911X (Sherpa/Romeo, impact factor)
Publisher Lippincott Williams & Wilkins
Extent 762-767
Origin https://doi.org/10.1161/01.HYP.34.4.762
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000083486500011
URI http://repositorio.unifesp.br/11600/43886

Show full item record




File

File Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Search


Browse

Statistics

My Account