Cardiovascular responses evoked by activation or blockade of GABA(A) receptors in the hypothalamic PVN are attenuated in transgenic rats with low brain angiotensinogen

Previous evidence indicates that a balance between inhibitory gabaergic and excitatory angiotensinergic factors in the PVN is important for cardiovascular control. We investigated the cardiovascular response evoked from activation or blockade of GABA(A) receptors in the paraventricular nucleus (PVN)...

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Bibliographic Details
Published in:Brain research 2012-04, Vol.1448, p.101-110
Main Authors: Gomes da Silva, Ana Quênia, Xavier, Carlos Henrique, Campagnole-Santos, Maria Jose, Caligiorne, Sordaini M, Baltatu, Ovidiu C, Bader, Michael, Santos, Robson Augusto S, Fontes, Marco Antônio P
Format: Article
Language:English
Subjects:
Angiotensinogen - deficiency
Animals
Antihypertensive Agents - pharmacology
Blood Pressure - drug effects
Brain Chemistry - drug effects
Brain Chemistry - genetics
GABA Agonists - pharmacology
GABA Antagonists - pharmacology
Gene Expression - drug effects
Heart Rate - drug effects
Hemodynamics - drug effects
Hemodynamics - physiology
Hexamethonium Compounds - pharmacology
Kidney - innervation
Kidney - physiology
Paraventricular Hypothalamic Nucleus - drug effects
Radioimmunoassay
Rats
Rats, Sprague-Dawley
Rats, Transgenic
Receptors, GABA-A - physiology
Sympathetic Nervous System - physiology
Transgenes - genetics
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Summary:Previous evidence indicates that a balance between inhibitory gabaergic and excitatory angiotensinergic factors in the PVN is important for cardiovascular control. We investigated the cardiovascular response evoked from activation or blockade of GABA(A) receptors in the paraventricular nucleus (PVN), in transgenic rats with low brain angiotensinogen [TGR(ASrAOGEN)]. Brain Ang II and Ang-(1-7) levels were also determined. In functional experiments, TGR(ASrAOGEN) and Sprague-Dawley rats (SD, control) were anesthetized with urethane and blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded. Brain Ang II and Ang-(1-7) levels were largely reduced in TGR(ASrAOGEN) compared with SD rats. Inhibition of PVN neurons with the GABA(A) agonist, muscimol (1 nmol/100 nL), resulted in an attenuated fall in all cardiovascular variables in TGR(ASrAOGEN) compared with SD rats. This difference was particularly pronounced in HR (TGR Mus -23±6 bpm vs. -77±9 bpm SD Mus; P
ISSN:1872-6240
DOI:10.1016/j.brainres.2012.02.021