Biomedical subjects

J Bugajski

Publications and source records attributed to J Bugajski.

At least 55 records · Page 3Linked to original sources

PubMed1994

Effect of corticotropin releasing hormone on the pituitary-adrenocortical activity under basal and social stress conditions.

The effect of social crowding stress on the CRH-induced hypothalamic-pituitary-adrenocortical (HPA) responsiveness was assessed in rats crowded for 3 days, when the HPA response to neurotransmitter receptors stimulation was powerfully reduced. CRH given systemically dose-dependently increased the secretion of corticosterone. The increase was not affected by pretreatment with prazosin or propranolol, an alpha 1- or beta-adrenergic receptor antagonist, indicating the lack of involvement of adrenergic receptors in that stimulation. In the corticosterone response to CRH administered icv, a moderate involvement of hypothalamic alpha 1-adrenergic receptors and neuronal noradrenaline seems possible. The corticosterone responses to CRH given by either route to rats exposed to social crowding stress were identical with the responses of unstressed controls. Our results for the first have time shown that social crowding stress does not impair the HPA responsiveness to CRH stimulation.

Animals↗

PubMed1994

Histaminergic components in carbachol-induced pituitary-adrenocortical activity.

The involvement of central histaminergic mechanisms in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by carbachol, a muscarinic cholinergic agonist, was investigated in conscious rats. The HPA activity was assessed indirectly, through corticosterone secretion. Carbachol given intracerebroventricularly elicited a dose-related increase in serum corticosterone levels. The corticosterone response to carbachol was totally abolished by systemic pretreatment 2h earlier with alpha-fluoro-methylhistidine (alpha-FMH), a specific inhibitor of brain histamine synthesis, which also significantly decreased histamine level in hypothalamus. Mepyramine, a histamine H1-receptor antagonist, moderately diminished the carbachol-induced corticosterone response and abolished the rise in hypothalamic histamine levels. Ranitidine a H2-receptor antagonist, considerably diminished the corticosterone response to carbachol but did not change the elevated hypothalamic histamine levels. Also atropine, a cholinergic antagonist, abolished the corticosterone response to carbachol, but did not significantly affect the carbachol-induced increase in hypothalamic histamine concentration. Ranitidine and atropine can directly block homologous hypothalamic receptors involved in CRF secretion. Partial inhibition of the carbachol-induced corticosterone secretion by mepyramine may be connected with prevention of the carbachol-induced increase in hypothalamic histamine content. These results suggest that hypothalamic histamine and histamine receptors are involved in the HPA stimulation by the muscarinic agonist carbachol.

Animals↗

PubMed1993

Calcium channel blockers impair the pituitary-adrenocortical responses to central adrenergic receptors stimulation.

The role of calcium channels in the hypothalamic-pituitary-adrenal (HPA) activity, stimulated by adrenergic receptor agonists was investigated indirectly through corticosterone secretion in conscious rats. The drugs were given intracerebroventricularly (icv) or intraperitoneally, calcium channel blockers 15 min before adrenergic receptor agonists. Verapamil and nifedipine considerably diminished the increase in serum corticosterone level induced by icv phenylephrine, an alpha 1-adrenergic receptor agonists. Verapamil almost completely suppressed the corticosterone response to icv clonidine, and alpha 2-adrenergic receptor agonist, and abolished the corticosterone response to the centrally administered isoproterenol, a beta-adrenergic agonist. The results demonstrate a significant role of calcium channels and calcium ions in the HPA activity, stimulated centrally by adrenergic receptor agonists. They also indicate that verapamil and nifedipine interfere predominantly with calcium channels on the hypothalamic CRH secreting neurons and anterior pituitary corticotrops when inhibiting pituitary-adrenocortical activity stimulated by adrenergic receptor agonists.

Adrenergic alpha-Agonists↗

PubMed1993

Social crowding stress diminishes the pituitary-adrenocortical and hypothalamic histamine response to adrenergic stimulation.

Social stress of crowding almost totally reduced the rise in serum corticosterone elicited by intracerebroventricular administration of isoprenaline, a beta-adrenergic receptor agonist, after 3 and 7 day of crowding and substantially diminished that response after 14 and 21 days. Crowding stress totally abolished the increase in hypothalamic histamine induced by isoprenaline in control rats. Crowding also significantly diminished the increase in serum corticosterone evoked by clonidine, an alpha 2-adrenergic agonist, and abolished the clonidine-induced elevation in hypothalamic histamine levels. The stimulatory effect of phenylephrine, an alpha 1-adrenergic agonist, on corticosterone secretion was only moderately diminished in crowded rats. Neither phenylephrine nor crowding stress changed significantly the hypothalamic histamine levels. These results indicate that social stress of crowding considerably impairs the hypothalamic-pituitary-adrenocortical responsiveness to central beta- and alpha 2-adrenergic receptor stimulation. Crowding also abolishes the rise in hypothalamic histamine induced by beta- and alpha 2-adrenergic agonist, suggesting a role of hypothalamic histamine in the HPA adaptation to the social stress of crowding.

Animals↗

PubMed1993

Central histaminergic mechanisms in the corticosterone response to clonidine.

Involvement of central histaminergic mechanisms in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by clonidine was investigated in conscious rats. Clonidine as well as adrenergic and histamine receptor antagonists were administered intracerebroventricularly (icv), the antagonists always 15 min prior to clonidine, and 1 h later the trunk blood was collected for corticosterone determination. alpha-Fluoromethylhistidine (alpha-FMH), a neuronal histamine synthesis inhibitor, was given ip 2 h before clonidine. Immediately after decapitation, brains were exposed and hypothalami were isolated on ice and frozen for further spectrofluorimetric histamine determination. The clonidine-induced increase in the serum corticosterone level was considerably, but not totally, reduced by icv or ip pretreatment with yohimbine, an alpha 2-adrenergic receptor antagonist. The rise in the corticosterone level induced by clonidine was significantly diminished by mepyramine, a histamine H1-receptor antagonist, and moderately lowered by cimetidine, a histamine H2-receptor antagonist. Clonidine significantly augmented the histamine content in the hypothalamus and rest of the brain. The clonidine-induced increase in hypothalamic histamine might be the cause of an increased corticosterone secretion via stimulation of central H1-histamine receptors. On the other hand, alpha-FMH injected 2 h before clonidine considerably diminished both the histamine content in the hypothalamus and the corticosterone secretion induced by clonidine. These results indicate that clonidine given centrally stimulates the HPA activity via not only alpha-adrenergic but also histaminergic mechanisms. Clonidine augments the hypothalamic histamine which, in turn, stimulates the corticosterone secretion, predominantly via histamine H1-receptors. Neuronal histamine is considerably involved in the stimulatory action of clonidine since inhibition of the neuronal histamine synthesis by alpha-FMH significantly depresses the corticosterone response to clonidine.

Animals↗

PubMed1992

Effect of gamma-aminobutyric acid and muscimol on corticosterone secretion in rats.

The effect of gamma-aminobutyric acid-receptor agonists, GABA and muscimol on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, and the receptors involved were investigated in conscious rats. GABA given ip induced a dual effect, in lower dose (10 mg/kg) it significantly decreased the resting serum corticosterone levels while in higher doses (100-500 mg/kg) it considerably raised that level. Muscimol (0.5 mg/kg ip) also increased the corticosterone concentration. Both GABA and muscimol given intracerebroventricularly (icv) induced a significant, dose-related increase in serum corticosterone levels. Bicuculline, a GABAA-receptor antagonist, totally abolished the corticosterone response to GABA but did not influence the response to muscimol. Pretreatment with atropine did not affect the corticosterone response to GABA but significantly diminished the response to muscimol. These results suggest that GABA moderately inhibits the pituitary-adrenal axis at the pituitary level but significantly stimulates it at the hypothalamic level. The stimulatory effect of GABA, but not muscimol, is mediated by hypothalamic GABAA-receptors, and in the effect of muscimol hypothalamic cholinergic, muscarinic receptors are involved to a significant extent.

Animals↗

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↗