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Information Journal Paper

Title

VASOPRESSIN MEDIATES THE CARDIOVASCULAR EFFECTS OF GABAERGIC SYSTEM IN THE BED NUCLEUS OF THE STRIA TERMINALIS

Pages

 Start Page 463 | End Page 469

Abstract

 Introduction: The nucleus bed of the stria terminalis (BST) is a part of the limbic system. Previous studies have shown that inhibition of GABA A receptor increases BLOOD PRESSURE and HEART RATE. This study was performed to find the possible mechanisms and circuits that mediate these responses.Materials and Methods: In 39 urethane-anesthetized male rats the femoral artery and vein were cannulated for recording the BLOOD PRESSURE and HEART RATE and drug injection respectively. Trachea was cannulated to ease ventilation, and bicuculline was unilaterally microinjected into the BST using micropipette. The maximum changes of mean arterial pressure (MAP) HEART RATE (HR) were compared with the preinjection values using the paired t-test.Results: Injection of bicuculline methiodide (BMI, 100 pmol/100 nl), a GABAA antagonist, caused a significant increase in the MAP (41.3±5.1 mmHg) as well as in the HR (33.2±5.6 beats/min). Administration (i.v.) of the muscarinic receptor blocker, homatropine methyl bromide had no effect on the magnitude of mean arterial pressure or HEART RATE responses to BMI, suggesting that the parasympathetic system is not involved in these responses. However administration (i.v.) of the nicotinic receptor blocker, hexamethonium bromide, althought it had no effect on the magnitude of mean arterial pressure response did abolish HEART RATE response to BMI, indicating that the sympathetic system is involved in the bradycardic effect of GABA. On the other hand, administration (i.v.) of a selective VASOPRESSIN V1 receptor antagonist abolished the pressor effect of BMI, which suggests that the GABAergic system of the BST decreases the arterial pressure via tonic inhibition of VASOPRESSIN release.Conclusion: We demonstrated, for the first time, that inhibition of GABAA, receptors increase BLOOD PRESSURE and HEART RATE via tonically inhibiting VASOPRESSIN release and sympathetic outflow to the heart.

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