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J Bugajski

Publications and source records attributed to J Bugajski.

At least 73 records · Page 4Linked to original sources
PubMed1988

Naloxone antagonizes a central histaminergic stimulation of corticosterone secretion in rats.

The interaction of central opioid receptors with histaminergic stimulation of the hypothalamo-pituitary-adrenocortical axis, evaluated indirectly through corticosterone secretion, was investigated in conscious unstressed rats. To avoid any possible direct action on the adrenal cortex, all drugs were given intracerebroventricularly (i.c.v.). Histamine, 2-pyridylethylamine (PEA), a histamine H1-receptor agonist, and 4-methyl-histamine (MeHA) and dimaprit, the H2-receptor agonists, considerably increased the serum corticosterone levels 1 h after administration. Naloxone, an opioid receptor antagonist, almost abolished the corticosterone response to PEA and considerably reduced the responses to MeHA, dimaprit and histamine. The maximum inhibitory effects of naloxone on corticosterone responses induced by histamine and histamine agonists were comparable with those of the H1- and H2-receptor antagonists, mepyramine and cimetidine. These results strongly suggest that a major part of the histaminergic stimulation of the hypothalamo-pituitary-adrenal axis is mediated by central opioid receptors.

Animals↗
PubMed1987

Hyperlipemic responses induced by centrally administered histamine H1- and H2-receptor agonists in rats.

The H1-receptor agonist 2-pyridylethylamine (PEA), and the H2-receptor agonists dimaprit and impromidine administered intracerebroventricularly (i.c.v.) to conscious rats considerably increased the concentration of free fatty acids (FFA) in the blood serum. The hyperlipemic effect of PEA was abolished by mepyramine, a H1-receptor antagonist. Responses to dimaprit and impromidine were not antagonized by cimetidine. These results suggest that central H1-receptor stimulation elicits the hyperlipemic responses in rats. The role of central H2-receptors in this reaction is not clear.

Animals↗
PubMed1987

Central histaminergic stimulation of corticosterone and hyperlipemic responses after chronic ethanol consumption in rats.

The consumption of ethanol in a 10% solution for 3 weeks produced a negligible increase in corticosterone secretion in the rat but raised the levels of free fatty acid (FFA) in the serum. Mepyramine insignificantly antagonized and cimetidine intensified the corticosterone response. Histamine and the H1- and H2-receptor agonists, 2-pyridylethylamine (PEA) and dimaprit significantly raised the serum corticosterone levels in chronically alcoholized rats. Mepyramine antagonized and cimetidine increased the ethanol-induced hyperlipemia. Histamine, PEA and dimaprit considerably increased the serum FFA levels in alcoholized rats. After withdrawal of ethanol, histamine and dimaprit induced a marked hyperlipemic effect, whereas PEA did not increase the serum FFA concentration. These results indicate that in chronically alcoholized rats the central histaminergic system interacts with ethanol in regulation of the serum FFA level. After the ethanol withdrawal central H1-receptors do not respond to H1-agonist stimulation.

Animals↗
PubMed1986

The interaction of ethanol with central histaminergic stimulation of the pituitary-adrenocortical and hyperlipemic activity.

Ethanol introduced intragastrically (i.g.) in rats increased the pituitary-adrenocortical activity, measured indirectly through corticosterone concentration in blood serum. Since this increase reached only about 40% of the maximum hormone levels observed in that species after another stimuli, ethanol may be considered as a relatively weak stimulus. Ethanol induced also a significant decrease in serum free fatty acid (FFA) levels which was blocked totally by a prior intracerebroventricular (i.c.v.) administration of either H1- or H2-histamine receptor antagonists, mepyramine or metiamide and cimetidine. The ethanol-induced increase in serum corticosterone was insensitive to a central histamine H1- and H2-receptors blockade. Ethanol abolished the rise in serum FFA levels induced by an i.c.v. administration of histamine, pyridylethylamine (PEA)-a H1-receptor agonist, and dimaprit--a H2-receptor agonist. The histamine- and histamine-agonists induced increases of serum corticosterone were generally slightly intensified by a prior i.g. administration of ethanol.

Animals↗
PubMed1985

Central histaminergic stimulation of hyperlipemic response in rats under stress.

In rats subjected to a mild stress of immobilization histamine, the H1-receptor agonist 2-pyridylethylamine (PEA), and the H2-receptor agonists 4-methyl histamine (4-MeHA) and impromidine administered intracerebroventricularly (i.c.v.) 1 h prior to stress, intensified the stress-induced increase in serum free fatty acid (FFA) levels. Impromidine was far more potent than histamine and its agonists in increasing hyperlipemia in stressed rats. The hyperlipemic response to histamine was abolished by i.c.v. pretreatment of rats with mepyramine, a H1-receptor antagonist, but was unchanged in rats pretreated with cimetidine or metiamide, H2-receptor antagonists. The increase in serum FFA levels induced in stressed rats by PEA was abolished by mepyramine but the hyperlipemic responses to 4-MeHA and impromidine were not antagonized by cimetidine. These results suggest that central H1-receptor mediate the histamine-stimulated hyperlipemic response in stressed rats.

Animals↗
PubMed1984

Interference of clonidine and alpha-methyl-p-tyrosine with stress and central histaminergic stimulation of the corticosterone response in rats.

In conscious rats clonidine given intracerebroventricularly 1 h prior to a mild stress of immobilization intensified the stress-induced increase of pituitary-adrenocortical response, measured indirectly through corticosterone concentration in blood serum. The corticosterone response to clonidine was abolished by i.c.v. pretreatment of rats with yohimbine, an alpha 2-adrenergic antagonist, and was antagonized by pretreatment with phenoxybenzamine, an alpha 1-adrenergic antagonist. Clonidine intensified also the corticosterone response induced in stressed rats by i.c.v. injected histamine, 2-pyridylethylamine (PEA), a H1-receptor agonist, and dimaprit, a H2-receptor agonist. The depletion of brain catecholamines by alpha-methyl-p-tyrosine (alpha-MT) considerably increased the corticosterone response to stress but did not substantially change the response to histamine, PEA and dimaprit in stressed rats. These results suggest that clonidine increases the corticosterone secretion induced by a mild stress and histamine and histamine H1 and H2 agonists mainly through the activation of central alpha 2-adrenoceptors. The increase by alpha-MT of the stress-induced corticosterone response may indicate the inhibitory role of central catecholamines in the pituitary-adrenocortical response to stress in rats.

Adrenergic alpha-Antagonists↗
PubMed1984

Effect of intracerebroventricular impromidine on pituitary-adrenocortical response to stress in rats.

In the rats subjected to a mild stress of immobilization impromidine, and H2-receptor agonist, given 60 min prior to the stress, intensified the stress-induced increase in hypophyseal-adrenocortical response, evaluated indirectly through the corticosterone concentration in the blood serum. Impromidine was far more potent but only about half as efficient as histamine, 4-methyl histamine (4-MH) and dimaprit. The effect of impromidine was abolished by pretreatment of the rats with cimetidine. The alpha-adrenergic blockers phenoxybenzamine, phentolamine and yohimbine, almost totally antagonized the corticosterone response to impromidine in stressed rats. Propranolol, a beta-adrenergic blocker, abolished the corticosterone response to impromidine but did not antagonize the response to 4-MH and dimaprit. The effect of impromidine was not modified by i.c.v. pretreatment of the rats with atropine. The results obtained show that impromidine is far more potent but less efficient than histamine and the previously known selective H2-receptor agonists in inducing the pituitary-adrenocortical response in stressed rats. These results also suggest that impromidine may release norepinephrine but not interact with cholinergic receptors while stimulating the corticosterone response in stressed rats.

Adrenal Cortex↗
PubMed1984

The effect of adrenergic and cholinergic antagonists on central histaminergic stimulation of pituitary-adrenocortical response under stress in rats.

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, alpha 1 and alpha 2-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 beta-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 alpha 1- and alpha 2-adrenergic receptors, but not beta-adrenergic and cholinergic muscarinic receptors interact with central H1 and H2 histaminergic stimulation of the increased pituitary-adrenocortical response in stressed rats.

Adrenal Cortex↗
PubMed1984

Effect of intracerebroventricular clonidine on serum corticosterone levels in rats.

In conscious, nonstressed rats clonidine given intracerebroventricularly (i.c.v.) increased the pituitary-adrenocortical response evaluated indirectly from corticosterone concentration. The maximum significant increase occurred 60 min after a dose of 10 micrograms. The alpha 2-adrenoceptor antagonist yohimbine given alone i.c.v. in low doses (0.05-1 microgram) had no effect on plasma corticosterone levels, but at higher doses (5 and 10 micrograms) it produced a significant rise in these levels. Phenoxybenzamine (0.05-10 micrograms, i.c.v.) caused a dose-related increase in corticosterone secretion. Pretreatment of rats with yohimbine considerably antagonized (up to 70%) the increase of corticosterone response induced by clonidine. Phenoxybenzamine failed to alter this effect. The depletion of brain catecholamines by alpha-methyl-p-tyrosine caused an increase in serum corticosterone concentration. The rise was suppressed by clonidine (10 micrograms, i.c.v.), and this suppression was antagonized in part by pretreatment with yohimbine. These data support the concept of the noradrenergic inhibition of ACTH secretion in rats. It seems likely that clonidine injected i.c.v. induces stimulation of corticosterone through the activation of presynaptic alpha 2-adrenoceptors and inhibition of noradrenaline release. The clonidine-induced inhibition of corticosterone after alpha-methyl-p-tyrosine seems to be mediated by alpha-adrenoceptors located postsynaptically.

Adrenocorticotropic Hormone↗
PubMed1983

Central histaminergic stimulation of pituitary--adrenocortical response in the rat.

In conscious rats histamine, the H1-receptor agonist 2-pyridylethylamine (PEA), and the H2-receptor agonists dimaprit and impromidine given intracerebroventriculary (i.c.v.) increased the hypophyseal-adrenocortical response, evaluated indirectly through the corticosterone concentration in the blood serum. On a molar basis histamine was the most potent drug whereas its agonists were less potent in inducing an increased corticosterone response. Impromidine however, was far more active than dimaprit and PEA. The effect of histamine was significantly yet not totally antagonized by either mepyramine, a H1-receptor antagonist, or cimetidine, a H2-receptor blocker. The combination of mepyramine and cimetidine caused a considerably stronger inhibition than that induced by either antagonist given separately. Mepyramine impaired the corticosterone response to PEA, and the responses to impromidine and dimaprit were significantly diminished by cimetidine. The results suggest that i.c.v. histamine increases the pituitary-adrenocortical activity via both H1- and H2-receptors, and there seems to be no significant prevalence of either of these receptors in mediating this action of histamine.

Animals↗
PubMed1983

The effect of clonidine injected centrally on serum-free fatty acids and glucose concentration in the rat.

Clonidine administered intracerebroventricularly (ICV) to conscious rats induced a significant dose-dependent increase in serum free fatty acid (FFA) and blood glucose levels. The rise in FFA and glucose concentrations after a dose of 10 micrograms averaged 80%-100% of the control levels. The alpha-adrenoceptor antagonists yohimbine, phentolamine, and phenoxybenzamine, administered alone ICV, did not substantially influence the control FFA and glucose levels. A hyperlipemic response to clonidine (10 micrograms) was abolished by an ICV pretreatment with yohimbine and was strongly antagonized by phentolamine but not by phenoxybenzamine. The clonidine-induced hyperglycemia was significantly diminished by phentolamine and only partly by yohimbine, whereas phenoxybenzamine was ineffective here. The histamine H2-receptor antagonist cimetidine, given ICV, failed to change these effects of clonidine. It seems likely that clonidine, given ICV, induces hyperlipemic and hyperglycemic effects through the stimulation of central alpha-adrenoceptors but not histamine H2-receptors. The lipolytic action of the drug depends more on the activation of alpha 2-adrenoceptors.

Animals↗
PubMed1983

Central H1- and H2-histaminergic stimulation of pituitary-adrenocortical response under stress in 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.

Animals↗
PubMed1983

Effect of metiamide, a histamine H2-receptor antagonist on reserpine-induced gastric ulcers and acid secretion.

The effect of metiamide on reserpine-induced gastric ulcers and on gastric secretion during 6 h after ip administration was investigated in conscious intact rats and in rats with chronic gastric fistula. Reserpine, 3 mg/kg ip increased substantially the concentration of gastric acid in the first 4 h. Metiamide given every 3 h in a low dose (0.01 mumol/kg) intensified reserpine-induced gastric ulcers and also significantly increased the reserpine-induced acid concentration and output. In larger doses, (50-100 mumol/kg) metiamide considerably diminished gastric ulcer development and decreased gastric acid concentration. Given every 2 h metiamide in doses of 50-100 mumol/kg almost completely abolished gastric ulcer formation and markedly reduced the secretion of gastric acid in reserpinized rats. Anti-ulcer effect of metiamide was stronger than its antisecretory action, suggesting also the antiulcer action of metiamide other than inhibition of acid secretion. The results suggest that in conscious rats histamine H2-receptors are involved in reserpine-induced gastric ulcer development and gastric acid secretion. The antiulcer effect of metiamide may in part depend on its antisecretory action.

Animals↗
PubMed1981

Lipolytic responses induced by intracerebroventricular administration of histamine in the rat.

Histamine (10-50 microgram) administered intraventricularly in conscious rats induced an increase in serum-free fatty acids. The maximum, significant increase appeared 30-60 min after administration. Histamine H1-receptor antagonists, mepyramine and chloropyramine, when injected 2 h prior to histamine, abolished considerably hyperlipaemic responses to histamine. H2-Receptor antagonists, metiamide and cimetidine, given i.c.v. only moderately diminished histamine-induced hyperlipaemia. Histamine injected i.c.v. also increased serum corticosterone levels considerably. This elevation was prevented significantly by the H1-receptor antagonist, mepyramine, but not by the H2-receptor blocker, cimetidine. It seems likely that histamine given i.c.v. induces lipolysis through the release of ACTH, one of the known lipid-mobilizing hormones. The central lipid-mobilizing mechanism after histamine depends more on activation of H1- than H2-receptors.

Animals↗
PubMed1981

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

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.

Animals↗
PubMed1981

The role of central histamine H1- and H2-receptors in hypothermia induced by histamine in the rat.

Histamine administered intraventricularly or into the anterior hypothalamic preoptic region induced dose-dependent hypothermia in rats with chronic i.c.v. cannula. This hypothermia was almost totally abolished by both the histamine H1- and H2-receptor antagonists, mepyramine or chloropyramine and metiamide or cimetidine, respectively, give i.c.v. prior to histamine. In behavioural thermoregulation studies histamine considerably diminished the mean duration of dwelling of the rat under the heat lamp. This effect was abolished by histamine H1- but not by H2-receptor antagonists. It is concluded that histamine induces hypothermia by lowering the set point of the hypothalamic thermostat by means of H1-receptors. Histamine H2-receptor blockers antagonized the increase in tail skin temperature after histamine administration, suggesting that h2-receptors are involved in a heat loss mechanism.

Animals↗