We studied the effects of the histamine H1 receptor antagonists diphenhydramine and pyrilamine, the H2 receptor antagonist ranitidine and the muscarinic receptor antagonist atropine injected into the third cerebral ventricle on prostaglandin F2α (PGF2α)-induced hyperglycemia in anesthetized fed rats. The concomitant injection of diphenhydramine (1 × 10–8, 5 × 10–8 mol) with 50 µg PGF2α significantly suppressed the increase in hepatic plasma glucose concentrations induced by PGF2α The concomitant injection of 1 × 10–8 mol pyrilamine with 50 µg PGF2α did not suppress the above-mentioned parameter, while 5 × 10-8 mol pyrilamine significantly suppressed it. Diphenhydramine suppressed the PGF2α-induced hyperglycemia to a greater extent than did pyrilamine. In contrast, concomitant injection of the H1 receptor antagonist ranitidine (1 × 10–8, 5 × 10–8 mol) did not suppress the hyperglycemia induced by PGF2α. The concomitant injection of 5 × 10–8 mol diphenhydramine or pyrilamine with 50 µg PGF2α significantly suppressed the increase in plasma epinephrine induced by PGF2α, but the same dose of ranitidine had no effect. The concomitant injection of atropine (5 × 10–8, 5 × 10–7 mol) with 50 µg PGF2α significantly suppressed the increase in hepatic plasma glucose and epinephrine induced by PGF2α. These findings demonstrate that PGF2α-induced hyperglycemia is mediated by the muscarinic receptors of cholinoceptive neurons and in part by H1 receptors in the central nervous system.

Keywords:
Brain, Histamine H1 receptor, H2 receptor, Muscarinic receptor, Hyperglycemia, Epinephrine, Prostaglandin F2α
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© 1992 S. Karger AG, Basel
1993
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