Biomedical subjects

J Bugajski

Publications and source records attributed to J Bugajski.

At least 55 records · Page 3Linked to original sources

PubMed1991

The significance of brain histamine and its receptors in opioid stimulation of the pituitary-adrenocortical activity.

The involvement of brain histamine, contained in mast cells and neurons, and central histamine receptors in stimulation of the pituitary-adrenal axis by opioids was investigated indirectly through corticosterone secretion in conscious rats. The opioid agonists leu-enkephalinamide (DADL), morphine and b-endorphin (b-End) the s- m- and putative e-opioid receptor agonists, given intracerebroventricularly (ici) induced a significant, dose-dependent increase in serum corticosterone levels. The corticosterone response to b-End and morphine was significantly impaired by pretreatment with mepyramine and cimetidine, whereas the response to DADL was insensitive to histamine antagonists. Twenty four hours after administration of compound 48/80 the corticosterone responses to the opioids were greatly diminished. Pretreatment with a-fluoromethylhistidine (a-FMH), a histamine synthesis inhibitor, almost abolished the corticosterone response to DADL, b-End and morphine. These results indicate that central neuronal histamine and histamine receptors are significantly involved in the opioid-induced stimulation of the pituitary-adrenal axis in rats.

Adrenal Cortex↗

PubMed1991

The intracerebroventricularly administered mast cells degranulator compound 48/80 increases the pituitary-adrenocortical activity in rats.

The effect of brain mast cells degranulation by compound 48/80 on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, and the involvement of a histaminergic mechanism in that stimulation was investigated in conscious rats. All the drugs were given intracerebroventricularly (icv), histamine antagonists 15 min prior to compound 48/80. Compound 48/80 induced a significant dose- and time-related increase in the serum corticosterone levels. That increase, measured 1 h after administration of compound 48/80, was moderately diminished by icv pretreatment of rats with mepyramine and cimetidine, histamine H1- and H2-receptor antagonists. Three hours after administration of compound 48/80 mast cells of the thalamus and the hypothalamus were completely degranulated. At the same time the thalamus and the whole brain histamine levels were substantially higher than in the saline-treated control rats. The above results suggest that histamine liberated from the brain mast cells and central histamine receptors play a moderate role in increasing the pituitary-adrenocortical activity by compound 48/80.

Adrenal Cortex↗

PubMed1991

The influence of alpha-fluoromethylhistidine and histamine receptor antagonists on the beta-endorphin-induced corticosterone response.

Involvement of a central histaminergic mechanism in the stimulating effect of beta-endorphin (beta-End) on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, was investigated in conscious rats. The rise in serum corticosterone levels, induced by beta-End injected intraventricularly (icv) was considerably impaired by pretreatment with naltrexone, an opioid receptor antagonist. The stimulating effect of beta-End was almost totally suppressed by a prior icv administration of mepyramine, a histamine H1-receptor antagonist, and also considerably reduced by pretreatment with cimetidine, an H2-receptor antagonist. The strongest suppression, by 83%; of the beta-End-induced corticosterone response was evoked by a prior administration of alpha-fluoromethylhistidine, an inhibitor of neuronal histamine synthesis in the brain. These results indicate that both the brain neuronal histamine and central histamine H1- and H2-receptors are considerably involved in the beta-endorphin-induced stimulation of the pituitary-adrenocortical activity.

Animals↗

PubMed1991

Alpha-fluoromethylhistidine decreases the Leu-enkephalinamide- and morphine-induced corticosterone response in rats.

The effect of inhibition of brain histamine synthesis by alpha-fluoromethylhistidine (alpha-FMH) on the pituitary adrenocortical activity stimulated by D-Ala-D-Leu-enkephalinamide (DADL) and morphine was investigated indirectly through corticosterone secretion in conscious rats. alpha-FMH (20 mg/kg i.p.) drastically reduced the whole brain histamine content, measured 2 h later. The same pretreatment also considerably reduced the corticosterone response to morphine given intraperitoneally. When alpha-FMH was administered intracerebroventricularly (50 micrograms), the maximum inhibition of the corticosterone response to DADL and morphine occurred 4 h after administration, which may suggest a weaker accessibility of alpha-FMH from the cerebral ventricle to the brain structures involved in pituitary-adrenocortical stimulation. The corticosterone responses were not related to the core temperature changes. These results indicate that inhibition of brain histamine synthesis by alpha-FMH considerably impairs the pituitary-adrenocortical response to the opioid delta- and mu-receptor agonists DADL and morphine. They also suggest that neuronal histamine is significantly involved in the central stimulation of the pituitary-adrenal axis by opioids.

Animals↗

PubMed1991

Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity.

The significance and site of adrenergic receptors involved in the control of the hypothalamic-pituitary-adrenal axis (HPA) activity was assessed indirectly by estimation of serum corticosterone levels 1 h after drug administration to conscious rats. Adrenergic drugs were given intracerebroventricularly (icv) and intraperitoneally (ip), the antagonists 15 min prior to the agonists. Noradrenaline, adrenalin and isoproterenol given by either route increased dose-dependently the serum corticosterone levels. The corticosterone response to icv noradrenaline was almost abolished by icv pretreatment with propranolol, a beta-adrenergic antagonist, and yohimbine, and alpha 2-receptor blocker, and was also considerably reduced by prazosin, an alpha 1-adrenergic antagonist. When given ip, these antagonists did not significantly influence the noradrenaline induced corticosterone response, which suggests a suprapituitary site of action of noradrenaline in stimulation of the HPA. The corticosterone response to icv adrenalin was suppressed by prazosin given by either route. The corticosterone response to ip adrenalin was almost abolished by pretreatment with yohimbine, and also significantly diminished by propranolol given by the same route. The increase in corticosterone secretion, induced by isoproterenol given by either route, was abolished by ip injection of propranolol. These results indicate that noradrenaline stimulates the HPA via alpha- and beta-adrenergic receptors, mainly at the suprapituitary level. Adrenalin increases that activity both via central and pituitary alpha- and beta-adrenoceptors. Isoproterenol activates the HPA by stimulation of pituitary beta-receptors.

Adrenergic alpha-Agonists↗

PubMed1990

Effects of systemic and intracerebroventricular phenylephrine and clonidine on corticosterone secretion in rats.

A site of action of adrenergic drugs and type of receptors involved in stimulating the pituitary-adrenocortical activity, assessed indirectly through corticosterone (CS) secretion, was investigated in conscious rats. Adrenergic drugs were administered intraperitoneally (i.p.) or intracerebroventricularly (i.c.v.), the antagonists always 15 min prior to the agonist and 1 h later the trunk blood was collected for CS determination. Phenylephrine (PHE) (alpha 1-agonist) given by either route increased dose-dependently the serum CS levels. Such effect of PHE given i.p. was abolished by i.p. pretreatment with prazosin (PRA) (alpha 1-antagonist), and similar effect of i.c.v. administered PHE was considerably suppressed by i.c.v. pretreatment with PRA. I.c.v. pretreatment with yohimbine (YO) (alpha 2-antagonist), did not influence the effect of PHE. Clonidine (CLON) given i.c.v. significantly increased the serum CS level and such effect was halved by i.c.v. pretreatment with either YO and PRA. I.p. administered PRA did not decrease the CLON-induced CS response. YO given i.p. considerably reduced the CLON-induced CS response in both low and high doses thus indicating the interaction with pre- and post-synaptic alpha-adrenoceptors. These results suggest that PHE activated the pituitary-adrenocortical axis by a selective stimulation of alpha 1-adrenoceptors located in the hypothalamus and possibly on anterior pituitary corticotrophs. CLON seems to stimulate the secretion of CS by activating both alpha 2- and alpha 1-adrenoceptors in the hypothalamus.

Animals↗

PubMed1989

Antagonistic action of naloxone on central histamine receptors-stimulated corticosterone secretion in rats under stress.

In rats under a mild stress of restraint the interaction between central opioid receptors and histaminergic stimulation of the pituitary-adrenocortical activity was investigated indirectly through corticosterone secretion. In order to avoid a possible direct action on adrenal glands, all the tested drugs were administered intracerebroventricularly (icv). Naloxone an opioid antagonist and cimetidine, a H2- and mepyramine a H1-receptor antagonists were given 15 min before histamine and histamine agonists. One hour after histaminergic drug injection the rats were restrained for 10 min and decapitated. Histamine, 2-pyridylethylamine (PEA), a histamine H1-receptor agonist, and 4-methylhistamine (MeHA) and dimaprit, H2-receptor agonists, significantly intensified the stress-induced increase in serum corticosterone levels. Naloxone, given alone icv or ip, did not substantially alter the stress-induced corticosterone response. Like mepyramine naloxone abolished the corticosterone response to PEA in stressed rats. Naloxone also decreased significantly, though not totally, the corticosterone response to MeHA, dimaprit and histamine, its efficiency being similar to that of cimetidine, a H2-receptor antagonist. These results suggest that in stressed rats central opioid receptors are considerably involved in the histamine H1-receptor - and, to a lesser degree, in the H2-receptor stimulation of the hypothalamo-pituitary-adrenocortical axis.

Animals↗

PubMed1988

Involvement of central histamine receptors in corticosterone secretion induced by intraventricular administration of morphine.

The effect of intracerebroventricular (i.c.v.) administration of morphine on corticosterone secretion was studied in conscious, unstressed rats. A dose-dependent increase in serum corticosterone levels was observed 1 h after morphine injection. The corticosterone response to morphine was antagonized in a dose-dependent manner, and at larger dose almost abolished, by i.c.v. pretreatment of rats with naloxone, an opioid receptor antagonist. Intraventricular pretreatment of rats with mepyramine and cimetidine, the histamine H1- and H2-receptor antagonists, significantly diminished the corticosterone response to morphine. These results suggest that central opioid receptors are involved in the stimulating effect of morphine on the hypothalamo-pituitary-adrenocortical axis. Central histamine H1- and H2-receptors seem to be substantially involved in the stimulatory effect of morphine on corticosterone secretion in conscious, unstressed rats.

Animals↗

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↗