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1

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

100%

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.

2

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

100%

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

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 4

3

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.

4

Nitric oxide and prostaglandins in the clenbuterol-induced ACTH and corticosterone secretion

100%

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 1

The present study was designed to determine the involvement of nitric oxide (NO) and prostaglandins (PG) in the stimulatory action of clenbuterol, a selective ß2-adrenergic receptor agonist on hypothalamic-pituitary-adrenal (HPA) axis under basal and social crowding stress conditions. Clenbuterol given i.c.v. (10 µg) or i.p. (0.2 mg/kg) considerably increased ACTH and corticosterone secretion. A selective ß2-receptor antagonist compound ICI 118551 and non-selective ß-receptor antagonist propranolol given by either route reduced the stimulatory action of clenbuterol. Crowding stress (21 rats in a cage for 7) for 3-7 days significantly reduced the i.c.v. clenbuterol-induced ACTH and corticosterone secretion and i.p. clenbuterol-elicited ACTH secretion. L-NAME, mainly endothelial nitric oxide synthase (NOS) blocker, stronger than L-NNA, a neuronal NOS blocker, reduced the clenbuterol-evoked ACTH and corticosterone secretion in control rats but did not significantly alter this secretion already reduced by crowding stress. Piroxicam, predominantly constitutive cyclooxygenase (COX-1) inhibitor, given i.p. significantly diminished the i.p. clenbuterol-induced ACTH and corticosterone secretion in control rats and tended to reverse the reduction of ACTH secretion by crowding stress. These results indicate that clenbuterol, a selective ß2-adrenoceptor agonist, is much stronger stimulator of the HPA axis than isoprenaline, a non-selective ß-receptor agonist. Social crowding stress reduces to a larger extent the HPA response to ß2-receptor stimulation. Likewise, in the HPA axis stimulation via ß2-adrenoceptors endogenous NO and prostaglandins are significantly involved. Beta2-adrenoceptor is a dominant functional subtype of ß-receptor in the stimulatory and modulatory signals regulating the HPA axis activity under basal and social stress conditions.

5

Effect of social stress on COX-1 and COX-2-induced alterations in the adrenergic agonists-evoked hypothalamic-pituitary-adrenal responses

100%

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

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,2

The purpose of the present study was to investigate the contribution of prostaglandins (PGs) synthesized by constitutive (COX-1) and inducible (COX-2) cyclooxygenase to stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists in rats under social crowing stress 3 days, (21 per a cage for 6) animals. The effects of phenylephrine, clonidine and isoprenaline, an alpha1-, alpha2- and ß-adrenergic agonist, respectively, in the presence and absence of COX-1 inhibitor, piroxicam, and COX-2 inhibitor, compound NS-398, on ACTH and corticosterone secretion in stressed rats were compared with these effects in non-stressed animals. All drugs were given intracerebroventricularly (i.c.v.), COX inhibitors 15 min before adrenergic agonists. Piroxicam (0.02 µg) and NS-398 (0.1 µg) significantly reduced the phenylephrine (30 µg) -induced ACTH and corticosterone secretion in both stressed and non-stressed rats. Piroxicam (0.02 µg) and NS-398 (0.01 µg) moderately decreased the clonidine (10 µg) -evoked hormone responses in control rats but did not alter these responses in stressed rats. Piroxicam (0.2 µg) and NS-398 (0.1µg) moderately diminished the isoprenaline (20 µg)-evoked ACTH and corticosterone response in control rats, while in stressed rats these inhibitors did not significantly alter the isoprenaline-induced rise in ACTH and corticosterone secretion. These results indicate that in hypothalamic structures involved in the regulation of adrenergic agonists-induced HPA stimulation COX-2 is expressed under physiological synaptic activity. Social crowding stress does not alter the significant involvement of prostaglandins in the HPA response induced by stimulation of central alpha1-adrenergic receptors. Prostaglandins are of lesser importance in activation of the HPA axis by alpha2-and ß-adrenergic receptors under basal and social stress conditions.

6

Environmental stress increases plasma tumor necrosis factor and decreases interferon gamma levels in rats

84%

Wrona D., Zander A., Slominska L., Grembecka B.

Acta Biologica Cracoviensia. Series Zoologia

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2008

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tom 50

29-36

7

Social stress impact on developmental stability of laboratory rat Rattus norvegicus

84%

Valetsky A. V., Dmitrieva I. L., Krushinskaya N. L., Zakharov V. M.

Acta Theriologica. Supplement

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1997

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nr 04

Developmental stability of the progeny of pregnant female rats Rattus norvegicus Berkenhout, 1769 kept under different conditions was studied. In two experimental groups, females were exposed to social stress by keeping them in crowded cages at different stages of pregnancy, from the 1st to the 15th and from the 16th to the 21th days, respectively. In the control group, pregnant females were kept under normal conditions. Fluctuating asymmetry of 20 skull characters (number of foramina for small blood vessels and nerves) was used as a measure of developmental stability. Variance of the difference in foramen number between the left and right sides of the skull (1-r) as well as mean number of asymmetrical traits per individual revealed an increase of fluctuating asymmetry in both experimental groups compared with the control group. These results imply the deterioration of developmental stability under impact of social stress.

8

Long-lasting effects of social stress on peritoneal inflammation in some strains of mice

84%

Scislowska-Czarnecka A., Chadzinska M., Pierzchala-Koziec K., Plytycz B.

Folia Biologica

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2004

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tom 52

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nr 1-2

9

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

84%

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 4,2

The present study examined the functional selectivity of nicotine for nicotinic acetylcholine receptors in the stimulation of the hypothalamic-pituitary-adrenal (HPA) axis, the effect of social crowding stress on HPA response to nicotine and the involvement of prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats crowded (24 per a box instead 7) for 7 days. Nicotine (2.5-5.0 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 h after administration. Mecamylamine (50 mg i.c.v.), a selective nicotinic receptor antagonist, atropine (0.1 mg/kg i.p.) a non-selective cholinergic receptor antagonist, or COX inhibitors were injected 15 min prior to nicotine and the rats were decapitated 1 h after the last injection. Mecamylamine abolished the nicotine-induced ACTH response and significantly diminished corticosterone response. Atropine did not alter ACTH response and modestly diminished corticosterone response to nicotine. Crowding stress significantly impaired the nicotine-evoked ACTH and corticosterone secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably diminished the nicotine-induced ACTH and corticosterone secretion in control and crowded rats. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker, did not markedly alter the nicotine-induced hormones secretion in either control or stressed rats. Indomethacin (2 mg/kg), a non-selective COX inhibitor diminished significantly, but to a lesser extent than piroxicam, the nicotine-stimulated ACTH and corticosterone response. These results indicate that systemic nicotine stimulates the HPA axis selectively via nicotinic acetylcholine receptors. Chronic social stress significantly impairs the nicotine stimulated ACTH and corticosterone secretion. Prostaglandins, generated by COX-1- but not by COX-2- isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion in both control and stressed rats.

10

Vascular function and nitric oxide production in chronic social-stress-exposed rats with various family history of hypertension

84%

Bernatova I., Csizmadiova Z., Kopincova J., Puzserova Z.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

The study investigated the effect of chronic crowding stress on vascular function and nitric oxide (NO) production in rats with various family history of hypertension. Wistar (W), wBHR (offspring of W dams and spontaneously hypertensive sires), sBHR (offspring of spontaneously hypertensive dams and W sires) and spontaneously hypertensive rats (SHR) were used. Twelve-week-old males were divided into the control or crowded group for eight weeks. Basal blood pressure (BP, determined by tail-cuff plethysmography) of W, wBHR, sBHR and SHR rats was 112 ± 3, 129 ± 2, 135 ± 2 and 187 ± 3 mmHg, respectively. Crowding increased BP and reduced aortic NO synthase activity only in sBHR and SHR rats, without alterations in hypothalamic NO production. Acetylcholine-induced vasorelaxation of the femoral artery of stress-exposed rats was improved in W, unaltered in wBHR and sBHR and reduced in SHR. Crowding reduced serotonin-induced vasoconstriction in W and wBHR rats but had no effect in sBHR and SHR rats. In conclusion, the results suggest that crowded offspring of normotensive mothers were able to modify their vascular function in order to maintain BP at normal levels. On the other hand, offspring of hypertensive mothers were unable of effective adaptation of vascular function in stressful conditions resulting in gradual development of hypertension.

11

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

84%

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.

12

The involvement of nitric oxide and prostaglandins in the cholinergic stimulation of hypothalamic-pituitary-adrenal response during crowding stress

84%

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

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 3

The aim of the present study was to determine the effect of social crowding stress and significance of nitric oxide (NO) and prostaglandins (PG) generated by constitutive and inducible nitric oxide synthase (NOS) and cyclooxygenase (COX) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic receptor agonist carbachol. Inhibitors of neuronal NOS (nNOS) L-NNA, general NOS L-NAME and inducible NOS (iNOS) aminoguanidine, as well as inhibitors of COX-1, piroxicam, and COX-2, compound NS-398 were administered 15 min prior to carbachol to control or crowded rats (24 rats in cage for 7, during 3 and 7 days). In stressed rats L-NAME, L-NNA and aminoguanidine significantly intensified the carbachol-induced ACTH and corticosterone secretion, like in control rats. Piroxicam, markedly decreased the carbachol-induced ACTH and corticosterone response under either basal or stress conditions. Compound NS-398 did not markedly alter the carbachol-induced HPA response in control and stressed rats. Crowding stress (3 days) significantly impaired the i.c.v. prostaglandin E2-induced ACTH response. Corticotropin releasing hormone (CRH) receptor antagonists, alpha-helical CRH [9-14], given i.c.v. did not alter the PGE2-evoked corticosterone response in either control or stressed rats, indicating that hypothalamic CRH is not involved in the PGE2-induced central stimulation of HPA axis. In control rats L-NAME considerably enhanced, while L-arginine, a physiological NOS substrate, abolished the PGE2-induced ACTH and corticosterone response. In stressed rats this NOS blocker significantly increased and L-Arg reduced the stimulatory effect of PGE2 on ACTH and corticosterone secretion. The carbachol-induced corticosterone response was significantly increased by pretreatment with nNOS inhibitor L-NNA and was considerably reduced by indomethacin, a general COX inhibitor. Pretreatment with both antagonists left the carbachol-induced corticosterone level unchanged, suggesting an independent and reciprocal effect of NO and PG in the cholinergic stimulation of pituitary-adrenocortical response. These results indicate that in the stimulatory action of muscarinic agonist, carbachol, NO is an inhibitory transmitter under basal and crowding stress conditions. This psychosocial stress does not functionally affect the NOS/NO systems. Prostaglandins are involved in the cholinergic muscarinic-induced stimulation of HPA response to a significant extent in non-stressed rats. PGE2 may be involved in the carbachol-elicited HPA response under basal and stress conditions. Prostaglandins released in response to muscarinic stimulation did not evoke the hypothalamic CRH mediation. NO significantly impairs and PG stimulates the carbachol-induced HPA response in rats under basal and social stress conditions.

13

Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress

84%

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

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 1

The aim of the present study was to determine the effect of social stress and 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 corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. The stressed rats were crowded in groups of 24 to a cage for 3 or 7 days, whereas the control animals were haused in groups of 7 to a cage of the same size. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. CRH administration. Inhibitors of COX-1, piroxicam (0.2, 2.0, and 5.0 mg/kg), and COX-2, compound NS-398 (0.2 and 2.0 mg/kg), were administered i.p. 15 min prior to CRH (0.1 µg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 3 and 7 days markedly intensifies the stimulatory action of CRH on ACTH secretion. Neither piroxicam nor NS-398 induce any significant effect on the CRH-elicited ACTH and corticosterone secretion in non-stressed or crowded rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the stimulation of HPA axis by CRH under either basal conditions or during crowding stress. These results also indicate that the stimulatory action of CRH on ACTH secretion is not only completely resistant to desensitization but is sensitized during social crowding stress. The results contrast with a significant involvement of PG in the vasopressin-induced stimulation of HPA response during crowding stress.

14

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

67%

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.

15

Social stress in laboratory rats Rattus norvegicus results in decreased immune competence of the offspring

67%

Pronin A. V., Nikolaeva T. N., Deyeva A. V., Zaytseva L. G., Vasil'eva E.I., Kirillicheva G. B., Baturina I. G., Solov'eva M.S., Zakharov V. M.

Acta Theriologica. Supplement

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1997

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nr 04

An immune system status of socially stressed laboratory rats Rattus norvegicus Berkenhout, 1769 and their offsprings was studied. Several tests on activity of the macrophages and lymphocytes as well as on the tumour necrosis factor a (TNFa) activity in the blood serum were used to assess an immune system status of the stressed and control groups of rats. The results indicated that social stress led to obvious alterations in the immune system of the stressed rats and especially of their offspring, where the changes were more pronounced.

16

Role of prostaglandins in the stimulation of the hypothalamic-pituitary-adrenal axis by adrenergic and neurohormone systems

59%

Bugajski J.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 4

17

Zdrowotne, immunologiczne i produkcyjne konsekwencje stresu

51%

Pomorska-Mol M.

Lecznica Dużych Zwierząt. Ogólnopolski Kwartalnik dla Lekarzy Weterynarii

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2018

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tom 13

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nr 1

Ograniczanie wyników

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

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

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

Nitric oxide and prostaglandins in the clenbuterol-induced ACTH and corticosterone secretion

Effect of social stress on COX-1 and COX-2-induced alterations in the adrenergic agonists-evoked hypothalamic-pituitary-adrenal responses

Environmental stress increases plasma tumor necrosis factor and decreases interferon gamma levels in rats

Social stress impact on developmental stability of laboratory rat Rattus norvegicus

Long-lasting effects of social stress on peritoneal inflammation in some strains of mice

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

Vascular function and nitric oxide production in chronic social-stress-exposed rats with various family history of hypertension

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

The involvement of nitric oxide and prostaglandins in the cholinergic stimulation of hypothalamic-pituitary-adrenal response during crowding stress

Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress

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

Social stress in laboratory rats Rattus norvegicus results in decreased immune competence of the offspring

Role of prostaglandins in the stimulation of the hypothalamic-pituitary-adrenal axis by adrenergic and neurohormone systems

Zdrowotne, immunologiczne i produkcyjne konsekwencje stresu