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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Inactivation of the DMH selectively inhibits the ACTH and corticosterone responses to hypoglycemia

Departments of ¹Psychiatry and Behavioral Sciences and ⁴Medicine, University of Washington, Seattle 98195-6560; and ³Division of Endocrinology/Metabolism and ²Geriatric Research, Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108

Submitted 16 July 2003 ; accepted in final form 22 September 2003

We have previously reported that repeated bouts of insulin-induced hypoglycemia (IIH) in the rat result in blunted activation of the paraventricular, arcuate, and dorsomedial hypothalamic (DMH) nuclei. Because DMH activation has been implicated in the sympathoadrenal and hypothalamic-pituitary-adrenal (HPA) responses to stressors, we hypothesized that its blunted activation may play a role in the impaired counterregulatory response that is also observed with repeated bouts of IIH. In the present study, we evaluated the role of normal DMH activation in the counterregulatory response to a single bout of IIH. Local infusion of lidocaine (n = 8) to inactivate the DMH during a 2-h bout of IIH resulted in a significant overall decrease of the ACTH response and a delay of onset of the corticosterone response compared with vehicle-infused controls (n = 9). We observed suppression of the ACTH response at time (t) = 90 and 120 min (50 ± 12 and 63 ± 6%, respectively, of control levels) and early suppression of the corticosterone response at t = 30 min (59 ± 13% of the control level). The epinephrine, norepinephrine, and glucagon responses were not altered by DMH inactivation. Our finding suggests that DMH inactivation may play a specific role in decreasing the HPA axis response after repeated bouts of IIH.

dorsomedial hypothalamus; stress; rat; lidocaine; hypothalamic-pituitary-adrenal axis

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