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Role of glutamate and angiotensin II receptors in the RVLM in chronic renal failure rats
Author(s) -
Dugaich Adriana Poli,
OliveiraSales Elizabeth Barbosa,
Carillo Bruno Arruda,
Abreu Nayda Parisio,
Boim Miriam Aparecida,
Bergamaschi Cassia Toledo,
Campos Ruy Ribeiro
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a738
Subject(s) - rostral ventrolateral medulla , medicine , endocrinology , angiotensin ii receptor type 1 , kynurenic acid , nitric oxide synthase , brainstem , glutamate receptor , angiotensin ii , candesartan , renin–angiotensin system , blood pressure , nitric oxide , receptor , heart rate
The aim of this study was to evaluate the role of the rostral ventrolateral medulla (RVLM) in the maintenance of hypertension and renal sympathetic nervous activity (RSNA) in a rat model of chronic renal failure (CRF). We also tested the expression of neuronal isoform of nitric oxide synthase (nNOS) and AT1 mRNA in the brainstem. Experiments were performed in male Wistar rats submitted to CRF by 5/6 nephrectomy. After 4 weeks of CRF induction, animals were anesthetized (urethane 1,4 g/Kg) for blood pressure (MAP), heart rate (HR) and RSNA recordings. Microinjections of Glutamate (10 nmol) into the RVLM increased MAP and RSNA in control rats more than in CRF (C, 46 ± 4 and CRF, 27 ± 4 mmHg; RSNA C 58% ± 6 and CRF 38% ± 4). Kynurenic acid into the RVLM did not change MAP and RSNA in both groups. However, inhibition of RVLM by GABA (0,5 M) decreased MAP in CRF rats more than in control rats (DCRF, 63 ± 8 and DC, 33 ± 3 mmHg). AT1 blockade in the RVLM by Candesartan (0,25; 0,5; 1,0 nmol) caused a pressor response and sympathetic activation in CRF and C. There was a downregulation of AT1 mRNA in CRF (C, 0,66 ± 0,09 and CRF, 0,16 ± 0,03 arbitrary unity‐AU) in the brainstem and an increase in the expression of nNOS mRNA (C, 0,7 ± 0,08 and CRF, 1,3 ± 0,06 AU). Taken altogether, the results suggest that the hypertension in CRF rats is dependent of sympathetic nervous system. Apparently, AT1 and glutamatergic receptors in the RVLM are not involved in the sympathetic activation in this model of hypertension. An increase in the oxidative stress in the brainstem is probably involved. Supported by CAPES, CNPq‐PRONEX.