The involvement of central histamine receptors in stress-induced responses of serum corticosterone and free fatty acids and in gastric ulcer development

Agents and Actions
J Bugajski, A Gadek

Abstract

Mild stress of restraint for 10 min at an ambient temperature of 18 degrees C increased serum corticosterone levels in rats considerably. Histamine given intravenously prior to restraint alone significantly further intensified the stress-induced elevation of serum corticosterone. Dimaprit and cimetidine failed to modify corticosterone responses to the mild stress. Severe stress of restraint and cold of 3 h duration increased serum corticosterone and free fatty acid levels considerably. Histamine given prior to stress exposure left the corticosterone and hyperlipaemic responses to severe stress unchanged. Dimaprit inhibited and cimetidine intensified the stress-induced hyperlipaemia. The most striking finding in the present experiment was a powerful inhibition of gastric stress ulcer generation by intraventricularly administered histamine. Dimaprit was similarly effective. This strong anti-ulcer effect of histamine was abolished by intraventricular pretreatment of rats with either H1- or H2-receptor antagonists, chloropyramine or cimetidine. The results may suggest that in the rat a mild stress does not fully activate central histaminergic pathways involved in corticosterone responses. During severe stress histamine considerably...Continue Reading

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Citations

Feb 24, 2001·Journal of Physiology and Biochemistry·O Martínez-AugustínF Sánchez de Medina
Feb 1, 1992·Pharmacology, Biochemistry, and Behavior·P GhiP Portaleone
Aug 1, 1983·Neuroscience·F Roberts, C R Calcutt
Nov 1, 1987·Pharmacological Research Communications·R Arrigo-Reina, C Spadaro
Jun 23, 1986·Life Sciences·I M Mazurkiewicz-Kwilecki, G D Prell

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