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A J Bugajski

Publications and source records attributed to A J Bugajski.

15 recordsLinked to original sources
PubMed1997

Mediation by nitric oxide of the carbachol-induced corticosterone secretion in rats.

Nitric oxide synthase, an enzyme responsible for nitric oxide (NO) formation has been found in the hypothalamic paraventricular nucleus and median eminence, structures closely associated with regulation of the pituitary activity, and the pituitary gland itself. Nitric oxide modulates the stimulated release of CRH from the rat hypothalamus in vitro, which suggests its role in regulating the secretion of ACTH from the pituitary corticotrops and of corticosterone from the adrenal cortex. The purpose of the present study was to elucidate the yet unknown role of endogenous NO in the HPA response to central cholinergic stimulation in conscious rats. Neither L-arginine an NO precursor, nor the NO synthase blockers N omega-nitro-L-arginine methyl ester (L-NAME) and N omega-nitro-L-arginine (L-NNA) caused any consistent changes in the basal serum corticosterone levels. L-arginine, given in higher doses (120-150 mg/kg ip) 15 min prior to icv carbachol (2 micrograms), markedly diminished the carbachol-induced rise in corticosterone secretion. Systemic pretreatment with the nitric oxide synthase inhibitor L-NAME (5 mg/kg) significantly raised the carbachol-elicited corticosterone response, while addition of L-arginine completely blocked the effect of L-NAME. A similar increase in the carbachol-induced corticosterone response was produced by icv pretreatment with L-NAME (2 micrograms), indicating a central site of the NO interaction with cholinergic stimulation of the HPA response. L-NAME is a weak inhibitor of neuronal NOS itself, and must first be de-estrified to N omega-nitro-L-arginine to potently inhibit this enzyme. Systemic (10 mg/kg) and icv (1 microgram) pretreatment with L-NNA enhanced more effectively the carbachol-induced rise in corticosterone secretion than did pretreatment with L-NAME by either route. These results are the first direct evidence that endogenous NO significantly inhibits the HPA response to central cholinergic, muscarinic receptor stimulation under in vivo conditions.

Animals↗
PubMed1996

Effect of indomethacin on the pituitary-adrenocortical response to adrenergic stimulation.

The role of prostaglandins (PGs) in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic agonists and catecholamines was investigated in nonanesthetized rats. The cyclooxygenase and PGs synthesis inhibitor indomethacin was given systemically or intracerebroventricularly (icv) 15 min prior to phenylephrine (30 micrograms), clonidine (10 micrograms), and isoproterenol (20 micrograms), an alpha 1-, alpha 2-, and beta-adrenergic receptor agonists, respectively, or noradrenaline (10 micrograms) and adrenaline (10 micrograms). Indomethacin given ip (2 mg/kg) or icv (10 micrograms) almost abolished the increase in corticosterone secretion elicited by phenylephrine, considerably reduced the response to clonidine but did not markedly affect the response to isoproterenol. Pretreatment with indomethacin by either route strongly suppressed the corticosterone response to noradrenaline, but did not substantially affect the hormonal response to adrenaline. The above data indicate that prostaglandins considerably mediate the HPA axis response to central stimulation of alpha 1- and alpha 2-, but not beta-adrenergic receptors. They also point to significant involvement of prostaglandins in the noradrenaline-, but not adrenaline-induced HPA axis predominantly via alpha 1-and alpha 2-adrenergic receptors, whereas adrenaline exerts stimulation manly via beta-adrenergic receptors.

Adrenal Cortex↗
PubMed1995

Crowding stress impairs the pituitary-adrenocortical responsiveness to the vasopressin but not corticotropin-releasing hormone stimulation.

To evaluate the effect of social crowding stress on the CRH and vasopressin-induced hypothalamic-pituitary-adrenocortical (HPA) response, both those neuropeptides were administered intracerebroventricularly and intraperitoneally to rats crowded for 3 days. Crowding stress did not affect the corticosterone response to CRH given by either route (1 micrograms i.c.v. or 2 micrograms/kg i.p.) but totally abolished or considerably diminished the response to vasopressin given i.p. (5 micrograms/kg) or i.c.v. (5 micrograms), respectively. Social crowding stress considerably impairs central vasopressin but does not change the CRH-system involved in the HPA stimulation.

Adrenocorticotropic Hormone↗
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

Effect of compound 48/80 on mast cells and biogenic amine levels in brain structures and on corticosterone secretion.

The effect of compound 48/80, given intracerebroventricularly, on mast cells (MC) and histamine, serotonin and noradrenaline levels in the hypothalamus, thalamus and hippocampus as well as on corticosterone secretion was investigated in rats. A relatively high amount of mast cells was found in the thalamus, a very low in the hypothalamus and almost none in the hippocampus. Compound 48/80 (1 and 5 micrograms) induced MC degranulation, a significant increase in corticosterone secretion and diminution of the thalamic histamine level. The drug also elicited small biphasic changes in histamine level in the hypothalamus and moderately increased serotonin turnover in the brain structures studied, but did not affect noradrenaline level in those structures. These results indicate that brain MC contain a significant amount of histamine, but not serotonin. Compound 48/80 releases histamine from MC, but does not markedly influence neuronal biogenic amines in the brain structures involved in regulation of the hypothalamic-pituitary-adrenal axis.

Animals↗
PubMed1994

Effect of isolation stress on brain mast cells and brain histamine levels in rats.

The effects of the chronic social stress of isolation on changes in brain mast cells (MC), the hypothalamic histamine content and the activity of the hypothalamic-pituitary adrenal (HPA) axis were investigated in rats. Social stress of isolation markedly reduced the total number of brain mast cells, most significantly by 90% in the first day. The extent of MC degranulation, 36-67%, in stressed rats did not significantly differ from that in control animals, 45-58%. Isolation stress substantially, though not significantly, increased the hypothalamic histamine content. The serum corticosterone levels in isolated rats did not significantly differ from the control levels. These results indicate that social stress of isolation considerably diminishes the number of brain MC and suggest that histamine which might be liberated from these cells does not significantly influence the HPA activity.

Animals↗
PubMed1994

Effect of compound 48/80 on the thalamic mast cells, serotonin level and corticosterone secretion in rats.

The effect of thalamic mast cells (MCs) degranulation and serotonin liberation by compound 48/80 on the hypothalamic-pituitary-adrenocortical (HPA) activity, measured indirectly through corticosterone secretion, was investigated in conscious rats. All drugs were given intracerebroventricularly (icv), the serotonin antagonists 15 min prior to compound 48/80. One hour after administration, compound 48/80 (1 and 5 micrograms) caused a significant increase in degranulated MC number in the thalamus, from control value of 20% up to 58%, and a considerable rise in the serum corticosterone level, but only minor diminution of the thalamic serotonin content. Pretreatment with methysergide, a serotonin receptor antagonist, only slightly dimished the compound 48/80-induced corticosterone response, while pretreatment with cyproheptadine, an antagonist of serotonin-histamine and cholinergic-receptors, significantly decreased the compound 48/80-elicited corticosterone response. These results show for the first time that thalamic mast cells contain a very small amount of serotonin, which may play only a minor role in increasing the HPA activity by compound 48/80. These findings also suggest that other mediators liberated from mast cells by compound 48/80 are responsible for the considerable increase in the HPA activity.

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

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↗