Biomedical subjects

A Gadek-Michalska

Publications and source records attributed to A Gadek-Michalska.

53 records · Page 3Linked to original sources

PubMed1995

Adrenergic regulation of the hypothalamic-pituitary-adrenal axis under basal and social stress conditions.

The significance of adrenergic neurons and anterior pituitary and hypothalamic adrenergic receptors in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) and vasopressin (AVP) was investigated under basal conditions and after three-days crowding stress in conscious rats. In nonstressed rats the corticosterone response to phenylephrine, an alpha 1-adrenergic receptor agonist, was totally abolished or considerably reduced by prazosin, an alpha 1-receptor antagonist, when both those drugs were given ip or icv, respectively. The corticosterone response to ip isoproterenol, a beta-adrenergic agonist, was abolished by icv or ip pretreatment with propranolol, a beta-adrenergic receptor antagonist. These results indicate involvement of functional alpha 1-adrenoceptors in the hypothalamus and anterior pituitary corticotrops and pituitary beta-adrenoceptors in stimulation of the HPA axis. AVP given ip was almost as potent as CRH in stimulating corticosterone secretion. The stimulatory effect of AVP given ip or icv on corticosterone secretion was significantly diminished by propranolol, but not prazosin or yohimbine, indicating an involvement of beta-adrenergic receptors. The specific noradrenergic neurotoxin DSP-4, given ip 11 days before the experiment, considerably diminished the hypothalamic noradrenaline (NA) level but did not influence the resting and icv CRH- or AVP-stimulated corticosterone secretion. In nonstressed rats CRH further enhanced significantly the DSP-4-elicited fall in hypothalamic NA, whereas AVP almost totally prevented that decrease. In stressed rats CRH considerably antagonized the DSP-4-induced decrease in the hypothalamic NA level while AVP did not affect that decrease. The CRH- and AVP-elicited changes in hypothalamic NA were not correlated with changes in corticosterone secretion. Tree-day crowding stress did not affect the CRH-induced corticosterone secretion, whereas it considerably reduced the AVP-evoked corticosterone response. These results indicate that pituitary and hypothalamic adrenergic receptors are significantly involved in the AVP- and CRH-induced HPA axis stimulation, but the hypothalamic NA level, though modified by these peptides, does not significantly influence the HPA response.

Adrenal Glands↗

PubMed1995

Influence of the central histaminergic systems on the pituitary-adrenocortical response to met-enkephalinamide.

A possible involvement of hypothalamic histamine and histamine receptors in the hypothalamic-pituitary-adrenocortical (HPA) activity stimulated by Met-enkephalinamide (DADM) was investigated indirectly by corticosterone secretion in conscious rats. DADM, a delta-opioid receptor agonist, given intracerebroventricularly (i.v.c.) induced a significant increase in the serum corticosterone level, which was considerably reduced by ip or icv pretreatment with naltrexone, an opioid antagonist. Pretreatment with alpha-fluoromethylhistidine (alpha-FMH) 20 mg/kg ip or 50 micrograms icv, an inhibitor of the brain histamine synthesis, drastically reduced the hypothalamic histamine level, did not affect the levels of noradrenaline and dopamine, and almost abolished the DADM-induced corticosterone response. Mepyramine and cimetidine, histamine H1- and H2-receptor antagonists, did not substantially change the corticosterone response to DADM. The present results suggest that DADM stimulates the HPA activity via central delta-opioid receptors. They also indicate that the reduction of the HPA response to DADM by alpha-FMH is connected with significant diminution of hypothalamic histamine, but not noradrenaline or dopamine levels. Central histamine receptors do not mediate the metenkephalinamide-induced HPA stimulation.

Adrenal Glands↗

PubMed1994

Effect of crowding on corticosterone responses to central adrenergic stimulation.

The social stress of crowding for 3, 7 and 14 days considerably reduced the increase in serum corticosterone elicited by intracerebroventricular administration of isoprenaline, a beta-adrenergic agonist, on the 3rd and 7th days of crowding. The corticosterone response to clonidine, an alpha 2-adrenergic agonist, was significantly diminished only after 3 days of crowding and this reduction was paralleled by a significant decrease in hypothalamic histamine content. The stimulatory effect of phenylephrine, an alpha 1-adrenergic agonist, was not significantly changed by crowding stress. Social crowding stress caused almost total and persistent reduction in the hypothalamic-pituitary-adrenocortical (HPA) responsiveness to noradrenaline which stimulates the HPA axis via both alpha- and beta-adrenergic receptors.

Animals↗

PubMed1994

Effect of social isolation on corticosterone secretion elicited by histaminergic stimulation.

The effects of social stress of isolation for 3, 7, and 14 days on the responsiveness of the hypothalamic-pituitary-adrenocortical (HPA) axis to the stimulation of central histamine receptors and on the contents of hypothalamic biogenic amines were investigated. The corticosterone response to intraventricular administration of pyridylethylamine (PEA), a histamine H1-receptor agonist, was significantly higher in isolated than in control rats. The corticosterone response to dimaprit, a histamine H2-receptor agonist, tended to be slightly weaker in the stressed rather than in control rats. PEA significantly diminished the hypothalamic noradrenaline, dopamine and serotonin contents in both control and isolated rats. Dimaprit also decreased the brain NA, but not the DA concentrations in control and isolated rats. The changes in monoamines were not correlated with either the time, direction or magnitude of changes in corticosterone levels. These results suggest that hyperresponsiveness of the HPA system to the stimulation of central H1-histamine receptors during social isolation may depend on changes in the efficacy of H1 receptors but not on changes in the brain monoamine levels.

Animals↗

PubMed1994

Pituitary-adrenocortical responsiveness to histaminergic stimulation during social stress of crowding in rats.

Social stress of crowding for 3, 7, 14 and 21 days drastically reduces the serum corticosterone response to intracerebroventricular administration of dimaprit, a histamine H2-receptor agonist, moderately diminishes the response to pyridylethylamine, an H1-receptor agonist, and does not change significantly the corticosterone response to histamine. These results suggest that social stress of crowding considerably desensitizes central histamine H2-receptors involved in stimulation of the hypothalamic-pituitary-adrenal axis.

Animals↗

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↗

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

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↗

PubMedDate not supplied

Effect of brain mast cells degranulation on the corticosterone response to stimulation of central opioid receptors in rats.

The influence of brain mast cells degranulation, exerted by compound 48/80 given intracerebroventricularly, on the opioid-induced stimulation of the pituitary-adrenal axis, measured indirectly through corticosterone secretion, was investigated in conscious rats. The mu- and delta-opioid receptor agonists Leu-enkephalinamide, morphine and beta-endorphin, given intracerebroventricularly, dose-dependently increased the serum corticosterone levels. The effect of Leu-enkephalinamide was not changed by pretreatment with the histamine H1- and H2-receptor antagonists mepyramine and cimetidine. When Leu-enkephalinamide, morphine and beta-endorphin were given 3 hr after compound 48/80, the serum corticosterone levels were higher than after either one of these drugs given separately, which suggests an independent mechanism of action. In rats pretreated 24 hr earlier with compound 48/80, i.e., when brain mast cells were completely degranulated, the stimulating effect of morphine was almost abolished and the effects of Leu-enkephalinamide and beta-endorphin were considerably reduced. Since the histamine levels in the whole brain and thalamus were elevated 3 and 24 hr after administration of compound 48/80, these results suggest that factors other than histamine depletion from brain mast cells by compound 48/80 may be responsible for the dramatic impairment of the stimulating effect of morphine, Leu-enkephalinamide and beta-endorphin on the pituitary-adrenal axis.

Animals↗