Wyniki wyszukiwania

1

Prostaglandins and nitric oxide regulate adrenocortical response to vasopressin in stressed rats

100%

Gadek-Michalska A., Bugajski J.

Acta Neurobiologiae Experimentalis

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1997

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tom 57

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nr 5

2

Effect of cyclooxygenase inhibitors on the vasopressin induced ACTH and corticosterone response during crowding stress

100%

Bugajski J., Gadek-Michalska A.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 2

The aim of the present study was to compare the effect of social stress on the corticotropin releasing hormone (CRH) and arginine vasopressin (AVP)-induced pituitary-adrenocortical activity. Also the significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by AVP under basal and crowding stress conditions was investigated. The control rats were housed 7 in a standard cage and stressed rats were crowded 24 in a cage of the same size during 7 days. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. AVP administration. Indomethacin (2.0 mg/kg i.p.), a non-selective COX inhibitor, piroxicam (0.2, 2.0, and 5.0 mg/kg), a more potent COX-1 than COX-2 inhibitor, and compound NS-398 (0.2 and 2.0 mg/kg) a selective COX-2 inhibitor, were administered i.p. 15 min prior to AVP (5.0 µg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 7 days considerably inhibits the stimulatory action of AVP on ACTH secretion, while it intensifies the CRH-induced ACTH secretion. Indomethacin, piroxicam and NS-398 significantly diminished the AVP-elicited ACTH and corticosterone secretion in non-stressed rats. None of these COX antagonist induced any significant inhibition of the AVP-induced ACTH and corticosterone secretion in stressed rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the HPA stimulation by AVP during crowding stress. These results suggest that social crowding stress desensitizes the PG stimulatory mechanism which considerably mediates the AVP-induced HPA stimulation under basal conditions. The results contrast with a lack of any involvement of PG in the CRH-induced stimulation of HPA response under basal or crowding stress conditions.

3

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

Nitric oxide (NO) is a major signaling molecule and biological mediator of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the role of NO formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS) in the stimulatory effect of nicotine on the HPA axis in rats under basal conditions. Also possible interaction of NOS systems with endogenous prostaglandins (PG) in that stimulation was assessed. NOS and cyclooxygenase inhibitors were administered i.p. 15 min prior to nicotine (2, 5 mg/kg i.p.). Plasma ACTH and serum corticosterone levels were measured 1 h after nicotine injection. NOS blockers given alone did not markedly affect the resting ACTH and corticosterone levels. L-NAME (2-10 mg/kg), a broad spectrum NOS inhibitor considerably and dose dependently enhanced the nicotine-induced ACTH and corticosterone secretion. L-NNA (2 mg/kg) and 7-nitroindazole (7-NI 20 mg/kg), neuronal NOS inhibitors in vivo also significantly augmented the nicotine-induced ACTH and corticosterone levels. L-arginine greately impaired the nicotine-induced hormone responses and reversed the L-NNA elicited enhancement of the nicotine-evoked ACTH and corticosterone response. In contrast to the constitutive eNOS and nNOS antagonists, an inducible NOS antagonist guanethidine (50-100 mg/kg i.p.) did not substantially affect the nicotine-elicited pituitary-adrenocortical responses. Indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase blocker abolished the L-NAME and L-NNA-induced enhancement of the nicotine-evoked ACTH and corticosterone response. These results indicate that NO is an inhibitory mediator in the HPA axis activity. Inhibition of its generation by eNOS and nNOS significantly enhances the nicotine-induced HPA response. Under basal conditions iNOS is not involved in the nicotine-induced ACTH and corticosterone secretion. Prostaglandins play an obligatory role in the response of HPA axis to systemic nicotine administration.

4

Nitric oxide mediates the interleukin-1beta- and nicotine induced hypothalamic-pituitary-adrenocortical response during social stress

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 3

We investigated the role of nitric oxide (NO) in the interleukin 1b (IL-1ß) and nicotine induced hypothalamic-pituitary-adrenal axis (HPA) responses, and a possible significance of CRH and vasopressin in these responses under basal and social stress conditions. Male Wistar rats were crowded in cages for 7 days prior to treatment. All compounds were injected i.p., nitric oxide synthase (NOS) inhibitors, a-helical CRH antagonist and vasopressin receptor antagonist 15 min before IL-1ß or nicotine. Identical treatment received control non-stressed rats. Plasma ACTH and serum corticosterone levels were measured 1 h after IL-1ß or nicotine injection. L-NAME (2 mg/kg), a general nitric oxide synthase (NOS) inhibitor, considerably reduced the ACTH and corticosterone response to IL-1ß (0.5 µg/rat) the same extent in control and crowded rats. CRH antagonist almost abolished the nicotine-induced hormone responses and vasopressin antagonist reduced ACTH secretion. Constitutive endothelial eNOS and neuronal nNOS inhibitors substantially enhanced the nicotine-elicited ACTH and corticosterone response and inducible iNOS inhibitor, aminoguanidine, did not affect these responses in non-stressed rats. Social stress significantly attenuated the nicotine-induced ACTH and corticosterone response. In crowded rats L-NAME significantly deepened the stress-induced decrease in the nicotine-evoked ACTH and corticosterone response. In stressed rats neuronal NOS antagonist did not alter the nicotine-evoked hormone responses and inducible NOS inhibitor partly reversed the stress-induced decrease in ACTH response to nicotine. These results indicate that NO plays crucial role in the IL-1ß-induced HPA axis stimulation under basal and social stress conditions. CRH and vasopressin of the hypothalamic paraventricular nucleus may be involved in the nicotine induced alterations of HPA axis activity. NO generated by eNOS, but not nNOS, is involved in the stress-induced alterations of HPA axis activity by nicotine.

5

Role of prostaglandins and nitric oxide in the lipopolysaccharide-induced ACTH and corticosterone response

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

This study was designed to determine the role of endogenous prostaglandins (PG) and nitric oxide (NO) in the lipopolysaccharide (LPS)-induced ACTH and corticosterone secretion in conscious rats. LPS (0.5 and 1 mg/kg) given i.p. stimulated the hypothalamic-pituitary-adrenocortical (HPA) activity measured 2 h later. A non-selective cyclooxygenase inhibitor indomethacin (10 mg/kg i.p.), piroxicam (2 mg/kg i.p.), a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (2 mg/kg i.p.), a selective inhibitor of inducible cyclooxygenase (COX-2) given 30 min before LPS (1 mg/kg i.p.) significantly diminished both the LPS-induced ACTH and corticosterone secretion. COX-2 blocker was the most potent inhibitor of ACTH secretion (72.3%). Nw-nitro-L-arginine methyl ester (L-NAME 2 and 10 mg/kg i.p.), a non-selective nitric oxide synthase (NOS) blocker given 15 min before LPS did not substantially alter plasma ACTH and corticosterone levels 2 h later. Aminoguanidine (AG 100 mg/kg i.p.), a selective inducible nitric oxide synthase (iNOS) inhibitor, considerably enhanced ACTH and corticosterone secretion induced by a lower dose (0.5 mg/kg) of LPS and did not significantly alter this secretion after a larger dose (1 mg/kg) of LPS. L-NAME did not markedly affect the indomethacin-induced inhibition of ACTH and corticosterone response. By contrast, aminoguanidine abolished the indomethacin-induced reduction of ACTH and corticosterone secretion after LPS. These results indicate an opposite action of PG generated by cyclooxygenase and NO synthesized by iNOS in the LPS-induced HPA-response.

6

Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

The purpose of the present study was to assess whether, and to what extent prior handling, restraint or social crowding stress during 3-10 days affects the hypothalamic-pituitary-adrenocortical (HPA) response to an acute short-lasting restraint stress. Also the effect of a feedback inhibitory mechanism of corticosterone in the impairment of HPA axis by these stressors was investigated. Male Wistar rats were pretreated with handling 1 min/day for 3-10 days, restraint 2 times daily for 3-7 days and crowding stress for 7 days before exposure to acute restraint stress in metal tubes for 10 min. Some group of rats received exogenous s.c. corticosterone either once 25mg/kg or 2 times daily 10 mg/kg for 3-10 days before restraint stress. After the last restraint the rats were decapitated and their trunk blood was collected for the measurement of plasma ACTH and serum corticosterone levels. Handling for 3-7 days, restraint for 3-7 days, and crowding for 7 days and a single pretreatment with corticosterone - all significantly and to a similar extent inhibited the restraint stress-induced increase in ACTH and corticosterone secretion. Chronic pretreatment with corticosterone blunted the restraint stress-induced increase in HPA axis activity. These results indicate that repeated short-lasting stress induced by handling, restraint, or crowding potently attenuates the acute restraint stress-induced stimulatory action of the HPA axis. They also indicate adaptive action of moderate stress on the HPA axis response to acute stress. The results also suggest that a short-lasting hypersecretion of corticosterone during psychological stress may induce a prolonged feedback inhibition of the HPA axis activity. The attenuation of HPA axis response by prior handling has also obvious methodological implications.

7

Nitric oxide in the adrenergic- and CRH-induced activation of hypothalamic-pituitary-adrenal axis

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 2

In this report we investigated the effect of 7-nitroindazole (7-NI), a specific neuronal inhibitor of nitric oxide synthase (nNOS) and L-NAME, a nonselective NOS inhibitor upon the adrenergic- and CRH-induced stimulation of the hypothalamic-pituitary-adrenal axis in nonanesthetized rast. 7-NI given i.p. and L-NAME administered i.c.v. considerably reduced ACTH and corticosterone secretion induced by phenylephrine (30 µg i.c.v.), an alpha1-adrenergic receptor agonist. These inhibitors also diminished the HPA response to isoprenaline (20 µg i.c.v.), a nonselective ß-adrenergic receptor agonist, and i.c.v. L-NAME significantly lowered the ACTH and corticosterone response to clenbuterol (10 µg i.c.v.), a selective ß2-adrenergic agonist. L-NAME abolished the noradrenaline (NA), an alpha- and ß-receptor agonist-evoked ACTH and corticosterone response, which was reversed by pretreatment with i.p. L-arginine, an endogenous NO substrate. 7-NI abolished the stimulatory action of corticotropin-releasing hormone (CRH 1 µg/kg i.p.) on ACTH but not corticosterone secretion. L-NAME only moderately diminished the CRH-induced ACTH secretion, suggesting that a major part of the CRH-induced HPA axis activation is of neuronal origin. Dihydropyridine, nifedipine, a specific L-type Ca2+ channel blocker, inhibited significantly the CRH-induced ACTH and corticosterone response in rats exposed to 3 days crowding stress but not in rats under basal conditions. This finding indicates the strategic importance of Ca2+ influx into the pituitary corticotrops to meet increased secretory requirement under stressful conditions. Collectively, our results point to complex functional relationship between NO, adrenergic agents CRH and Ca2+ in the regulation of HPA axis activity.

8

The significance of central adrenergic system in the met-enkephalin-induced corticosterone secretion

81%

Glod R., Gadek-Michalska A., Olowska A., Bugajski J.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 5

9

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

81%

Gadek-Michalska A., Bugajski A. J., Bugajski J.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 3

563-575

We investigated the role of interleukin-1ß (IL-1ß) and prostaglandins (PG) in the 1-adrenergic agonist, phenylephrine-induced hypothalamic-pituitary-adrenal axis (HPA) responses under basal and social stress conditions. Male Wistar rats, either control or exposed to crowding stress for 7 days prior to treatment, were used in these experiments. All compounds were injected i.p. Cyclooxygenase COX-1 and COX-2 inhibitors, piroxicam and compound NS-398, IL-1ß and IL-1ß receptor antagonist (IL-1ßRA) were injected 15 min before phenylephrine. Plasma ACTH and serum corticosterone levels were measured 1 h after phenylephrine or IL-1ß injection. Phenylephrine, in respective higher dose administered systemically (0.4 mg/kg i.p.) was almost equally effective as given i.c.v. (30 µg) in stimulating ACTH and corticosterone secretion. Likewise, the extent of the involvement of PG generated by COX-1 and COX-2 in the phenylephrine-induced ACTH and corticosterone secretion was similar after systemic or i.c.v. treatment under both resting and stress conditions. Piroxicam, stronger than compound NS-398, reduced the i.p. phenylephrine-induced ACTH and corticosterone secretion. IL-1ß receptor antagonist (50 µg/kg i.p.) did not significantly affect the inhibitory action of piroxicam on the i.p. phenylephrine-induced ACTH and corticosterone secretion in control rats, but significantly enhanced the inhibition evoked by piroxicam in stressed rats. IL-1ß (2.5 µg/kg i.p.) significantly increased ACTH and corticosterone secretion under basal conditions. Crowding stress for 7 days markedly impaired the IL-1ß-induced ACTH and corticosterone secretion. The mechanism of the stimulatory action of i.p. IL-1ß, which does not cross the blood-brain barrier, may comprise both central and peripheral components of the HPA axis. These results suggest that under basal conditions IL-1ß is not markedly involved in the 1-adrenergic agonist-induced stimulation of the HPA axis activity. During social crowding stress IL-1ß and prostaglandins are significantly involved in this stimulation.

10

Nitric oxide and prostaglandins in the lipopolysaccharide-indiuced pituitary-adrenal response during stress

81%

Gadek-Michalska A., Spyrka J., Bugajski J.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

11

Chronic stress adaptation of the nitric oxide synthases and IL-1beta levels in brain structures and hypothalamic-pituitary-adrenal axis activity induced by homotypic stress

81%

Gadek-Michalska A., Tadeusz J., Rachwalska P., Bugajski J.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 3

12

Repeated restraint stress alters glutamatergic but not gabaergic transmission within the paraventricular nucleus of the hypothalamus

81%

Kusek M., Tokarski K., Gadek-Michalska A., Hess G.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

The hypothalamic paraventricular nucleus (PVN) plays a key role in the activation of the hypothalamic-pituitary-adrenal axis (HPA) in response to stressors. Wistar rats were subjected to restraint lasting 10 min and repeated twice daily for 3 days. Brain slices were prepared 24 h after the last restraint session and studied ex vivo. Whole-cell patch-clamp method was used to record spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) from presumed parvocellular neurosecretory neurons in slices containing a part of the PVN. Repeated restraint stress resulted in an increase in the mean frequency of sEPSCs and in a decrease in the rise time and the decay time constant of sEPSCs. There were no changes in the mean amplitude of sEPSC. All measured parameters of sIPSCs remained unaltered. The relationship between the injected current and the spiking rate of parvocellular neurons was reduced. These data indicate that restraint stress, repeated for 3 days, selectively enhances the excitatory inputs to parvocellular neurons of the PVN, most likely via a combination of pre- and postsynaptic mechanisms. These changes are accompanied by a decrease in the intrinsic excitability of PVN neurons. Support: “DeMeTer” and statutory funds from the Institute of Pharmacology.

13

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Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity

81%

Bugajski J., Turon M., Gadek-Michalska A., Borycz J. A.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 1

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 intraperito neally (ip), the antagonists 15 min prior to the agonists. Noradrenaline, adrenalin and isoproterenol given by either route increased dosedependently the serum corticosterone levels. The corticosterone response to icv noradrenaline was almost abolished by icv pretreatment with propranolol, a ß-adrenergic antagonist, and yohimbine, an α₂ -receptor blocker, and was also considerably reduced by prazosin, an α₂- 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 α and ß-adrenergic receptors, mainly at the suprapituitary level. Adrenalin increases that activity both via central and pituitary a and ß-adrenoceptors. Isoproterenol activates the HPA by stimulation of pituitary ß-receptors.

14

Effect of subdiaphragmatic vagotomy and cholinergic agents in the hypothalamic-pituitary-adrenal axis activity

81%

Bugajski A. J., Zurowski D., Thor P., Gadek-Michalska A.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 2

In the present study, we examined whether the vagus nerve is involved in mediating the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic and nicotinic agonists, carbachol and nicotine. The site of HPA axis muscarinic stimulation was determined using peripheral (i.p.) and intracerebroventricular (i.c.v.) administration of carbachol, atropine sulphate (AtrS) and atropine hydrobromide (AtrBr). The i.p. carbachol-(0.5 mg/kg)-induced corticosterone response was significantly reduced by i.p. pretreatment with AtrBr (0.1 mg/kg), but was not diminished by i.c.v. AtrS (0.1µg). The increase in corticosterone secretion induced by i.c.v. carbachol (2 µg) was totally abolished by i.c.v. pretreatment with AtrS (0.1 µg) but was not altered by i.p. AtrBr. Subdiaphragmatic vagotomy performed 2 weeks earlier substantially decreased the i.p. carbachol (0.2 mg/kg)-induced ACTH response and markedly augmented ACTH and corticosterone response to a higher dose of carbachol (0.5 mg/kg) in comparison with the responses in sham operated rats. Vagotomy abolished the stimulatory effect of i.p. nicotine in a low dose (1 mg/kg) on ACTH and corticosterone secretion; the ACTH response to higher dose (2.5 mg/kg) was considerably reduced, while corticosterone response remained unaffected. These results suggest that carbachol given i.c.v. evokes considerable corticosterone response by stimulation of central cholinergic muscarinic receptors. A major part of the i.p. carbachol-induced corticosterone secretion results from peripheral cholinergic muscarinic receptor stimulation. Subdiaphragmatic vagotomy moderately intensified the carbachol-induced ACTH and corticosterone secretion. Vagotomy significantly reduced the nicotine-induced ACTH secretion, possibly by the involvement of vagal afferents. The nicotine-induced corticosterone secretion is not exclusively regulated by circulating ACTH but by various intra-adrenal regulatory components.

15

Influence of nitric oxide synthase inhibitors on the vasopressin-induced pituitary-adrenocortical activity and hypothalamic catecholamine levels

81%

Bugajski J., Gadek-Michalska A., Glod R., Borycz J.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 4

16

Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress

81%

Bugajski J., Gadek-Michalska A., Bugajski A. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Acetylcholine potently stimulates the hypothalamic-pituitary-adrenal (HPA) axis. Cholinergic receptor agonist carbachol, given intraperitoneally (i.p.) or into the lateral cerebral ventricle (i.c.v.) to non-anesthetized rats acts via multiple pathways to stimulate the HPA axis. The present study sought to determine 1) the functional selectivity of carbachol for cholinergic muscarinic and/or nicotinic receptors involved in the stimulation of HPA axis; 2) the involvement of prostaglandins (PGs) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the carbachol-induced ACTH and corticosterone secretion in non-stressed rats and animals exposed to social crowding stress for 7 days (24 per a cage for 6). Carbachol was given i.c.v. or i.p. and cholinergic receptor antagonists or cyclooxygenase isoenzyme antagonists were given by the same routes 15 min earlier. One hour after the last injection trunk blood was taken for ACTH and corticosterone determinations. Atropine (0.1 µg i.c.v.), a cholinergic receptor antagonist, totally abolished the carbachol (2 µg i.c.v.)-induced ACTH and corticosterone secretion and mecamylamine (20 µg i.c.v.), a selective nicotinic receptor antagonist, did not affect this secretion. This finding indicates that carbachol functions as a selective central cholinergic muscarinic receptor agonist for the HPA axis stimulation. Crowding stress significantly diminished the carbachol (0.2 mg/kg i.p.)-induced plasma ACTH and corticosterone levels measured 1 hr after administration. Pretreatment with indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase inhibitor, significantly diminished the ACTH and corticosterone responses to carbachol (0.2 mg/kg i.p.) in control rats and moderately decreased these responses in stressed rats. Piroxicam (0.2 and 2.0 mg/kg i.p.), a COX-1 inhibitor, considerably impaired the carbachol-induced ACTH and corticosterone responses in control rats and markedly diminished these responses in stressed rats. A selective COX-2 blocker, compound NS-398 (0.2 and 2.0 mg/kg i.p.), substantially decreased the carbachol-induced hormones secretion in control rats but did not markedly alter this secretion in stressed rats. These results indicate that in the carbachol-induced HPA axis activation PGs generated by COX-1 are considerably and to a much greater extent involved than PGs generated by COX-2. Social stress markedly diminishes the mediation of PGs generated by COX-1 but PGs synthesized by COX-2 do not substantially participate in the carbachol-induced HPA response.

17

Psychosocial stress affects the involvement of prostaglandins and nitric oxide in the lipopolysaccharide-induced hypothalamic-pituitary-adrenal response

81%

Gadek-Michalska A., Spyrka J., Bugajski J.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 2

The role of prostaglandins and nitric oxide (NO), generated after peripheral lipopolysaccharide (LPS) administration, in the adaptation of hypothalamic-pituitary-adrenal (HPA) axis under stressful circumstances remains to be elucidated. The aim of the present study was to assess the effect of chronic repetitive restraint or social crowding stress on the involvememt of nitric oxide and prostaglandins in the LPS-induced pituitary-adrenocortical response. Male Wistar rats were restrained in metal tubes 2x10 min/day or crowded in cages for 7 days prior to treatment. All compounds were injected i.p., cyclooxygenase (COX) and nitric oxide synthase (NOS) inhibitors 15 min before LPS. Two hrs after injection LPS induced a significant increase in ACTH and corticosterone secretion. Repeated restraint impaired more potently than crowding stress the LPS-induced HPA-response. Indomethacin, a non-selective COX inhibitor, considerably reduced the LPS-induced HPA response in non-stressed rats and to a lesser extent diminished this response in repeatedly restrained or crowded rats. Neuronal NOS inhibitor, Nw-nitro-L-arginine decreased the LPS-induced HPA response, more potently in control than crowded rats. Aminoguanidine, an iNOS inhibitor, diminished the LPS-elicited ACTH response in crowded rats. These results indicate that prostaglandins and NO generated by neuronal and inducible NOS are involved in the LPS-induced HPA axis response under basal conditions and during its adaptation to chronic social stress circumstances.

18

Central histaminergic mechanism in the corticosterone response to clonidine

81%

Bugajski J., Gadek-Michalska A., Borycz J., Bugajski A. J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 3

19

Involvement of the central noradrenergic system in cholinergic stimulation of the pituitary-adrenal response

81%

Bugajski J., Borycz J., Gadek-Michalska A.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 2

20

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

81%

Bugajski J., Gadek-Michalska A., Borycz J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 4

Ograniczanie wyników

Prostaglandins and nitric oxide regulate adrenocortical response to vasopressin in stressed rats

Effect of cyclooxygenase inhibitors on the vasopressin induced ACTH and corticosterone response during crowding stress

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

Nitric oxide mediates the interleukin-1beta- and nicotine induced hypothalamic-pituitary-adrenocortical response during social stress

Role of prostaglandins and nitric oxide in the lipopolysaccharide-induced ACTH and corticosterone response

Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress

Nitric oxide in the adrenergic- and CRH-induced activation of hypothalamic-pituitary-adrenal axis

The significance of central adrenergic system in the met-enkephalin-induced corticosterone secretion

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

Nitric oxide and prostaglandins in the lipopolysaccharide-indiuced pituitary-adrenal response during stress

Chronic stress adaptation of the nitric oxide synthases and IL-1beta levels in brain structures and hypothalamic-pituitary-adrenal axis activity induced by homotypic stress

Repeated restraint stress alters glutamatergic but not gabaergic transmission within the paraventricular nucleus of the hypothalamus

Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity

Effect of subdiaphragmatic vagotomy and cholinergic agents in the hypothalamic-pituitary-adrenal axis activity

Influence of nitric oxide synthase inhibitors on the vasopressin-induced pituitary-adrenocortical activity and hypothalamic catecholamine levels

Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress

Psychosocial stress affects the involvement of prostaglandins and nitric oxide in the lipopolysaccharide-induced hypothalamic-pituitary-adrenal response

Central histaminergic mechanism in the corticosterone response to clonidine

Involvement of the central noradrenergic system in cholinergic stimulation of the pituitary-adrenal response

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