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GABAA AND GABAB RECEPTOR-MEDIATED INHIBITION OF SYMPATHETIC OUTFLOW IN THE PARAVENTRICULAR NUCLEUS IS BLUNTED IN CHRONIC HEART FAILURE

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SUMMARY



Alterations in the paraventricular nucleus (PVN) are reported to be involved in sympathetic overactivity in chronic heart failure (CHF). Inhibitory inputs into the PVN contribute to sympathetic outflow. The aim of the present study was to comparatively determine the role of GABA mechanisms in the PVN in the tonic control of cardiovascular activity in anaesthetized sham and CHF rats.



The CHF model was induced by coronary artery ligation. Unilateral microinjection of the GABAA receptor agonist muscimol (0.1–0.8 nmol/200 nL) or the GABAB receptor agonist baclofen (0.25–2.0 nmol/200 nL) into the PVN produced similar, dose-dependent reductions in arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA). This response was significantly blunted in CHF rats. In contrast, microinjection of the GABAA receptor antagonist bicuculline (25–200 pmol/200 nL) or the GABAB receptor antagonist CGP35348 (0.25–2.0 nmol/200 nL) into the PVN caused larger, dose-dependent increases in AP, HR and RSNA in sham than in CHF rats.



Polymerase chain reaction data showed that mRNA expression levels of the GABAA receptor α1-subunit and of the GABAB1(a) and GABAB1(b) receptor subtypes in the PVN were significantly lower in CHF than in sham rats.



The results of the present study suggest that the tonic inhibition mediated by both GABAA and GABAB receptors in the PVN on sympathetic outflow is blunted in CHF, which may be an important mechanism responsible for sympathetic hyperactivity in CHF.
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Keywords: GABA; microinjection; polymerase chain reaction; renal sympathetic nerve activity; sympathoexcitation

Document Type: Research Article

Publication date: May 1, 2009

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