Vasopressin mediates the cardiovascular effects of GABAergic system in the bed nucleus of the stria terminalis

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. 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. 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. 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

[ role of estrogen on cardiovascular response due to GABA and glutamate receptors in Rostral ventromedial medulla in ovarictomized rats]

The Rostral Ventromedial Medulla [RVMM] is one of the nuclei controlling cardiovascular system. This study was performed to determine the effects of 17beta-estradiol [E], on the GABA and Glutamate cardiovascular responses of RVMM of female rats. Experiments were performed on 40 anaesthetized and paralyzed rats, divided into two groups of ovarictomized [OVX] and ovarictomized-estrogen treated [OVX+E] rats. Drugs [50 nl] bicuculline methiodide [BMI] an antagonist GABAA receptor [1 mM], phaclophen an antagonist GABAA receptor [5mM], and kynurenic acid a nonselective antagonist glutamate receptors [5 mM], were microinjected by micropipette into the RVMM using stereotaxic system. Blood pressure and heart rate were recorded before and throughout each experiment. The means of maximum changes of mean arterial pressure and heart rate were compared between groups of OVX and OVX+E and saline using ANOVA. In the OVX+E group, estrogen decreased the mean arterial blood pressure [P<0.05] and heart rate [P<0.001] compared to those of OVX group. Microinjection of BMI resulted in an increase of heart rate [HR] with no significant effect on the blood pressure [BP] in both OVX and OVX+E, but the increase of HR was significantly higher than in the OVX+E group [p<0.05]. Microinjection of phaclophen and kynurenic acid had no significant effect on HR and BP in either the OVX or the OVX+E group; not did microinjection of saline have any significant effects on HR and BP. The present data suggest that estrogen decreased the mean arterial blood pressure and heart rate, and in the RVMM of female rats augments the inhibitory effect of the GABAergic system on the heart rate via the GABAA receptors