A possible interaction of central histaminergic receptors with adrenergic and cholinergic muscarinic neurons in increasing the pituitary-adrenocortical response under stress, assessed indirectly from the corticosterone concentration in blood serum, was investigated in conscious rats. All the drugs were administered intracerebroventriculary, the antagonists 15 to 30 min prior to the agonists. The histamine-induced increase in serum corticosterone levels of stressed rats was considerably antagonized by prazosin, phenoxybenzamine, phentolamine and yohimbine, α₁ and α₂-adrenergic antagonists. These antagonists abolished or significantly attenuated the corticosterone response to 2-pyridylethylamine (PEA), an H₁-receptor agonist, and to dimaprit and 4-methylhistamine(4-MeHA), H₂-receptor agonists. Propranolol, a β-adrenergic blocker, did not substantially change the corticosterone response induced by histamine or histamine H₁- and H₂-receptor agonists. Similarly, atropine was ineffective in blocking the increase in serum corticosterone responses induced by either histamine or PEA and dimaprit in stressed rats. These results suggest that both α₁- and α₂-adrenergic receptors, but not β-adrenergic and cholinergic muscarinic receptors interact with central H₁ and H₂ histaminergic stimulation of the increased pituitary-adrenocortical response in stressed rats.

In rats subjected to a mild stress of immobilization histamine, H₁-receptor agonist 2-pyridylethylamine (PEA), and H₂-receptor agonists, 4-methylhistamine (4-MHA) and dimaprit, given intraventricularly 60 min prior to stress, intensified the stress-induced increase of hypophyseal-adrenocortical response, evaluated indirectly through corticosterone concentration in blood serum. The effects were dose dependent and on a molar basis histamine and PEA were the most potent and 4-MHA and dimaprit were less effective, in this respect. The effect of histamine was almost totally blocked by both H₁-receptor antagonists, mepyramine or chloropyramine, and by H₂-receptor antagonists, metiamide or cimetidine. The corticosterone response to PEA was abolished by mepyramine, and the responses to 4-MHA or dimaprit were antagonized by cimetidine and metiamide. The response to the H₁ agonist was not substantially altered by pretreatment with cimetidine, and the responses to the H₂ agonists were not changed by mepyramine. These results suggest that in stressed rats the corticosterone response to histamine is mediated by both H₁ and H₂ central histamine receptors.

No 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 prevents gastric ulcer generation and both H1- and H2-receptors mediate this action of histamine.

O-Glycans from pig gastric mucin were released by beta-elimination in 0.2 M triethylamine and 50% aqueous hydrazine solution. The released glycan hydrazides were isolated using Centricon 10 separators, brought to their reducing form and reductive by labelled with p-aminobenzoic acid ethyl ester (ABEE). Labelled products were fractionated into neutral and acid fractions on a Bio-Gel P4 column, calibrated with a mixture of dextran oligosaccharides, labelled according to the same procedure.