Previous studies have shown that: (1) activation of neurons in the dorsomedial hypothalamus (
DMH) of the rat by blockade of local GABAA receptors with
bicuculline methiodide (BMI) elicits cardiovascular changes resembling those seen in experimental stress, including marked sympathetically-mediated
tachycardia, and (2) inhibition of neurons in the same region by local microinjection of the GABAA receptor agonist
muscimol can virtually abolish stress-induced
tachycardia. This study examined the possibility that GABAB receptors exist in the neural circuitry of the
DMH, and that stimulation of these receptors might suppress the cardiovascular response to local disinhibition with BMI. Microinjection of BMI 10 pmol into the
DMH in
urethane-anesthetized rats resulted in marked
tachycardia with little or no effect on arterial pressure. Simultaneous injection of the GABAB receptor agonist
baclofen at doses of 2.5, 5.0 and 10 pmol produced dose-related suppression of BMI induced
tachycardia. Coinjection of the GABAB receptor antagonist
2-hydroxysaclofen 100 or 200 pmol had no significant effect on the heart rate response to BMI, but reversed the suppression elicited in the presence of
baclofen. These findings indicate that (1) functional GABAB receptors exist in the
DMH, and (2) stimulation of these receptors inhibits the
tachycardia resulting from blockade of local GABAA receptors.