Knigge U, Matzen S, Warberg J
Institute of Medical Physiology C, Panum Institute, University of Copenhagen, Denmark.
Endocrinology. 1990 Mar;126(3):1430-4. doi: 10.1210/endo-126-3-1430.
The involvement of hypothalamic histaminergic neurons in the stress-induced release of peripheral catecholamines was studied in conscious, freely moving male rats. Blood samples were obtained via a catheter in a femoral artery. Intracerebroventricular infusion of histamine (HA; 30 micrograms) increased the plasma concentrations of norepinephrine (NE) and epinephrine (E) 3- and 9-fold, respectively. The plasma level of dopamine was not affected. The effect of HA was prevented by prior intracerebroventricular infusion of the H1-receptor antagonist mepyramine (100 micrograms) or the H2-receptor antagonist cimetidine (100 micrograms). Restraint stress applied for 5 min caused an immediate but transient increase in the plasma concentrations of NE and E which were increased 5- and 11-fold, respectively. The plasma level of dopamine was not altered significantly by restraint stress. The effect of stress on NE and E was almost prevented by prior icv infusion of mepyramine or cimetidine. The HA receptor antagonists had no effect on the basal plasma catecholamine level. We conclude that neuronal HA is an important mediator of the restraint stress-induced release of peripheral catecholamines by an action on H1- and H2-receptors within the central nervous system.
