Disinhibition of rostral raphe pallidus neurons increases cardiac sympathetic nerve activity and heart rate.

We determined the cardiovascular effects of microinjecting the GABA(A) receptor antagonist, bicuculline, into the rostral raphe pallidus (RPa) on arterial pressure (AP), heart rate (HR) and cardiac sympathetic nerve activity (CSNA) in urethane-chloralose anesthetized, artificially-ventilated rats. In 26 animals, microinjection of the GABA(A) receptor antagonist, bicuculline (2 mM, 30 nl), into RPa increased CSNA (+234+/-64% of control), HR (+91+/-10 bpm) and mean AP (+16+/-3 mmHg). A similar tachycardia was evoked after removal of both adrenal glands, but was absent after beta-adrenergic receptor blockade with atenolol. Equivalent percentage increases in CSNA and HR were evoked by disinhibition of the rostral RPa neurons after inhibition of cardiovascular sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) with bilateral microinjections of the GABA(A) receptor agonist, muscimol (6 mM, 50 nl) which markedly lowered CSNA, HR and AP. These results indicate that RPa contains a population of neurons, possibly sympathetic premotor neurons with direct projections to spinal cardiac sympathetic preganglionic neurons, that receive a tonic, GABAergic inhibition and thus do not contribute markedly to resting levels of CSNA and HR, but when disinhibited, they can produce large increases in CSNA and HR comparable to those seen during certain stress responses.