CORONARY VASOCONSTRICTOR PATHWAY FROM ANTERIOR HYPOTHALAMUS INCLUDES NEURONS IN RVLM

We have previously identified discrete brain sites [anterior (AHA) and lateral hypothalamus, periaqueductal gray, pontine parabrachial nucle us, lateral reticular formation, and rostral ventrolateral medulla (RV LM)] in the cat, in which electrical or chemical activation produces c oronary vasoconstriction. This study examines whether the most rostral (AHA) and caudal (RVLM) of these sites are connected as part of a com mon pathway mediating coronary vasoconstriction. In chloralose-anesthe tized cats, electrical stimulation in the AHA produced maximum increas es in arterial pressure (41 +/- 10%) and coronary vascular resistance (28 +/- 9%). Microinjection of lidocaine into the RVLM attenuated the increases in arterial pressure (10 +/- 3%) and coronary vascular resis tance (5 +/- 1%) in response to electrical stimulation in the AHA (P < 0.05 vs. before lidocaine). Lidocaine nonspecifically inhibits neural elements in the region. Gamma-Aminobutyric acid in the RVLM, which se lectively inhibits cell bodies and not fibers passing through the RVLM , attenuated the increase in coronary vascular resistance (38 +/- 8 to 14 +/- 3%; P < 0.05) but not the increase in arterial pressure (87 +/ - 12 to 92 +/- 16%) in response to electrical stimulation in the AHA. These data indicate that coronary vasoconstriction in response to elec trical stimulation in the AHA requires cell bodies in the RVLM; howeve r, the associated pressor response is mediated by fibers passing throu gh the RVLM. We conclude that a polysynaptic descending pathway that m ediates sympathetic coronary vasoconstriction descends from the AHA th rough a synaptic connection in the RVLM.