Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2003;42:707-712
Published online before print August 11, 2003, doi: 10.1161/01.HYP.0000086524.35251.2D
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
42/4/707    most recent
01.HYP.0000086524.35251.2Dv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Carvalho, T. H. F.
Right arrow Articles by Campos, R. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Carvalho, T. H. F.
Right arrow Articles by Campos, R. R.
Related Collections
Right arrow Animal models of human disease

(Hypertension. 2003;42:707.)
© 2003 American Heart Association, Inc.


Scientific Contributions

Role of Endogenous Angiotensin II on Glutamatergic Actions in the Rostral Ventrolateral Medulla in Goldblatt Hypertensive Rats

Taís Helena F. Carvalho; Cássia T. Bergamaschi; Oswaldo U. Lopes; Ruy R. Campos

From Federal University of São Paulo, School of Medicine, São Paulo, Brazil.

Correspondence to Ruy R. Campos, PhD, Universidade Federal de São Paulo, Escola Paulista de Medicina, Rua Botucatu 862, 04023-060, São Paulo, SP, Brazil. E-mail campos{at}fcr.epm.br

In this study, we investigated the cardiovascular responses mediated by rostral ventrolateral medulla neurons (RVLM) in the Goldblatt hypertension model (2K-1C) treated or not treated with captopril. The actions of glutamate into the RVLM were tested, injecting glutamate (0.1 mol/L, 100 nL) and its antagonist kynurenic acid (0.02 mol/L, 100 nL). Glycine (0.5 mol/L, 100 nL) was also microinjected. Experiments were performed in male Wistar rats (weight, 250 to 300 g); 5 groups were studied: (1) 2K-1C nontreated (H, n=6); (2) 2K-1C treated with captopril, 10 mg/kg per day (Ht10, n=10); (3) 2K-1C treated with captopril, 50 mg/kg per day (Ht50, n=7); (4) control normotensive rats (N, n=7); and (5) normotensive rats treated with captopril, 50 mg/kg per day (Nt50, n=8). All experiments in 2K-1C were performed 6 weeks after renal surgery; captopril treatment lasted for the last 2 weeks. In urethane-anesthetized rats (1.2 g/kg IV), bilateral microinjection of glycine into the RVLM caused a depressor response; there was no difference between groups in relation to the change of variation (N: 54±2; H: 46±12; Ht10: 50±3, and Ht50: 42±7 mm Hg). Only in the H group, kynurenic acid microinjection into the RVLM caused a depressor response (H: 158±8 to 132±8 mm Hg). Glutamate response was larger in hypertensive than in normotensive rats (N: 38±2.6 and H: 55±6); no difference was observed between hypertensive groups. The data suggest that glutamate acts tonically to drive the RVLM in 2K-1C rats, and this action is modulated by endogenous angiotensin II. The increase in the glutamate actions within the RVLM may contribute to the pathogenesis of renovascular hypertension.


Key Words: brain • angiotensin • captopril • amino acid • sympathetic nervous system




This article has been cited by other articles:


Home page
J. Physiol.Home page
P. M. Sonner, J. A. Filosa, and J. E. Stern
Diminished A-type potassium current and altered firing properties in presympathetic PVN neurones in renovascular hypertensive rats
J. Physiol., March 15, 2008; 586(6): 1605 - 1622.
[Abstract] [Full Text] [PDF]