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L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

By using L-glutamate as a physiological tool to selectively stimulate neurons in specific subnuclear regions of the nucleus tractus solitarius (NTS), we have sought to differentiate those regions that modulate cardiovascular activity from those that modulate gastric activity. Microinjections of L-glutamate (300 pmol/25 nl) into the dorsomedial NTS of alpha-chloralose-anesthetized rats elicited dose-dependent falls in arterial pressure (AP) of 37.5 +/- 7.7 Torr from a base line of 130 +/- 5.8 Torr and gastric pressure (GP) of 0.8 +/- 0.1 cmH2O and inhibited the usual 5-6 waves/min phasic activity. Microinjection into the ventromedial NTS did not affect AP but transiently lowered GP by 1.6 +/- 0.2 cmH2O and eliminated phasic waves. The GP changes were vagally mediated. Microinjections into the area postrema or the hypoglossal nucleus elicited neither AP nor GP changes. Microinjections in other NTS areas at the same rostral-caudal level did not alter GP consistently. This study suggests that local stimulation of neurons in a specific region of the NTS elicits vagally mediated alterations of tonic GP and phasic activity and that AP and GP can be influenced independently in the medial NTS region.