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Biomedical subjects

A Gadek-Michalska

Publications and source records attributed to A Gadek-Michalska.

At least 19 recordsLinked to original sources
PubMed2002

Effect of adrenergic antagonists and cyclooxygenase inhibitors on the nicotine-induced hypothalamic-pituitary-adrenocortical activity.

Nicotine is a potent stimulus for the hypothalamic-pituitary-adrenal (HPA) axis. Systemic nicotine acts via central mechanisms to stimulate by multiple pathways the release of ACTH from the anterior pituitary corticotrops and corticosterone from the adrenal cortex. Nicotine may stimulate indirectly the hypothalamic paraventricular nucleus, the site of the corticotropin-releasing hormone (CRH) neurons which activates ACTH release. In the present studies an involvement of adrenergic system and prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats was investigated. Nicotine (2.5-5 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 hr after administration. Adrenergic receptor antagonists or COX inhibitors were injected i.p. 15 min prior to nicotine and the rats were decapitated 1 hr after the last injection. Prazosin (0.01-0.1 mg/kg), an alpha1-adrenergic antagonist, significantly decreased the nicotine-evoked ACTH and corticosterone secretion. Yohimbine (0.1-1.0 mg/kg), an alpha2-adrenergic antagonist, moderately diminished ACTH response, and propranolol (0.1-10 mg/kg), a beta-adrenergic antagonist, did not significantly alter the nicotine-induced hormones secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably impaired the nicotine-induced ACTH and corticosterone secretion. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker did not markedly alter these hormones secretion, and indomethacin (2 mg/kg), a non-selective COX inhibitor significantly diminished ACTH response. These results indicate that systemic nicotine stimulates the HPA axis indirectly, and both adrenergic system and prostaglandins are significantly involved in this stimulation. Noradrenaline, stimulating postsynaptic alpha1-adrenergic receptors, and prostaglandins, synthesized by COX-1 isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion.

Adrenal Cortex↗
PubMed2001

A single corticosterone pretreatment inhibits the hypothalamic-pituitary-adrenal responses to adrenergic and cholinergic stimulation.

The purpose of the present study was to determine whether an increased plasma corticosterone or dexamethasone levels induced by a single corticosterone or dexamethasone injection to conscious rats affects the hypothalamic-pituitary-adrenocortical (HPA) activity induced by adrenergic and cholinergic agonists. Male Wistar rats were pretreated subcutaneously (s.c.) with a single dose of dexamethasone (5 mg/kg) or corticosterone (25 mg/kg) 24 or 48 h before intraperitoneal (i.p.) administration of adrenergic agonists: phenylephrine, an alpha1-adrenergic receptor agonist, clenbuterol, a beta2-adrenergic agonist and noradrenaline acting predominantly on alpha1-adrenoreceptors, and cholinergic agonists: carbachol, a predominant muscarinic receptor agonist and nicotine, a nicotinic receptor agonist. Dexamethasone profoundly decreased the resting ACTH levels in control rats and given 24 h before each of the stimulatory agonist abolished the adrenergic- and cholinergic agonists-induced ACTH and corticosterone responses. Pretreatment with corticosterone of control rats did not substantially alter the resting plasma ACTH and serum corticosterone levels measured 24 and 48 h later. A single pretreatment with corticosterone abolished or powerfully inhibited, perhaps by a feedback mechanism, the ACTH and corticosterone responses induced 24 and 48 h later by all adrenergic and cholinergic agonists used in this study. These results indicate that prolonged administration of corticosterone is not necessary to induce almost complete suppression of the HPA responsiveness to adrenergic or cholinergic stimulation. Chronic treatment with corticosteroids to achieve glucocorticoid receptors desensitization does not seem to be required.

Adrenergic Agonists↗
PubMed2001

Involvement of constitutive (COX-1) and inducible cyclooxygenase (COX-2) in the adrenergic-induced ACTH and corticosterone secretion.

The involvement of prostaglandins synthesized by constitutive (COX-1) and inducible cyclooxygenase (COX-2) in central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists was investigated in conscious rats. COX-1 and COX-2 inhibitor, piroxicam (0.02 and 0.2 microg) and compound NS-398 (0.01 and 0.1 microg), respectively, were given intracerebroventricularly (i.c.v.) 15 min prior to i.c.v. adrenergic receptor agonists: phenylephrine (30 microg) and clonidine (10 microg), an alpha1- and alpha2-adrenergic agonist, and isoprenaline (20 microg) a non-selective beta-adrenergic agonist and clenbuterol (10 microg) a selective beta2-adrenergic agonist. Piroxicam and NS-398 considerably and dose-dependently reduced the phenylephrine-induced increase in ACTH and corticosterone secretion. Pretreatment with piroxicam and NS-398 markedly impaired the clonidine-evoked ACTH and corticosterone secretion. Piroxicam moderately diminished the isoprenaline-elicited increase in ACTH and corticosterone, while NS-398 did not markedly alter ACTH secretion. The clenbuterol-induced ACTH and corticosterone responses were considerably impaired by pretreatment with piroxicam, and slightly less potently by NS-398. These results indicate that in central structures involved in regulation of the HPA axis both constitutive and inducible cyclooxygenase are present under normal conditions in rats. These isoenzymes are significantly involved in the stimulatory signaling transduced by postsynaptic alpha1-adrenergic receptors and, to a lesser extent, by alpha2-adrenergic receptors. Both isoenzymes affect moderately the stimulatory action of a non-selective beta-adrenergic agonist on ACTH and corticosterone secretion. COX-1 participates considerably and COX-2 markedly in the potent stimulatory action of selective beta2-adrenergic receptors on HPA axis.

Adrenocorticotropic Hormone↗
PubMed2001

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

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 beta-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 microg) and NS-398 (0.1 microg) significantly reduced the phenylephrine (30 microg) -induced ACTH and corticosterone secretion in both stressed and non-stressed rats. Piroxicam (0.02 microg) and NS-398 (0.01 microg) moderately decreased the clonidine (10 microg) -evoked hormone responses in control rats but did not alter these responses in stressed rats. Piroxicam (0.2 microg) and NS-398 (0.1 microg) moderately diminished the isoprenaline (20 microg) -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 beta-adrenergic receptors under basal and social stress conditions.

Adrenocorticotropic Hormone↗
PubMed2000

The influence of indomethacin on the acth secretion induced by central stimulation of adrenergic receptors.

We had previously demonstrated that indomethacin affected the corticosterone secretion induced by central stimulation of alpha-but not beta-adrenergic receptors in conscious rats. In the present study we investigated whether hypothalamic and/or pituitary prostaglandins (PGs) were involved in the central adrenergic stimulation of ACTH secretion. Indomethacin, 2 mg/kg ip or 10 microg intracerebroventricularly (icv), was administered 15 min before phenylephrine (30 microg icv), an alpha-adrenergic agonist, clonidine (10 microg), an alpha2-adrenergic agonist, and isoprenaline (20 microg) or clenbuterol (10 microg), a beta1- or beta2-adrenergic agonist. One hour after the last injection the rats were decapitated and plasma levels of ACTH were measured. The present results show that the ACTH responses induced by icv administration of phenylephrine and clonidine were considerably impaired by icv or ip pretreatment with indomethacin, an inhibitor of prostaglandin synthesis. Indomethacin given by either route only slightly diminished the isoprenaline-induced ACTH response and did not substantially alter the clenbuterol-induced response. The adrenergic-induced ACTH responses were more potently inhibited by ip than by icv pretreatment with indomethacin, which may result from a stronger inhibition of PGs synthesis in the median eminence and anterior pituitary by ip pretreatment with indomethacin than in hypothalamic structures by its icv administration. These results indicate a significant involvement of PGs in central stimulation of the hypothalamic-pituitary adrenal (HPA) axis by alpha1- and alpha2- but not beta-adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed1999

Social stress inhibits the nitric oxide effect on the corticotropin-releasing hormone- but not vasopressin-induced pituitary-adrenocortical responsiveness.

Putative involvement of endogenous nitric oxide (NO) in the corticotropin-releasing hormone (CRH, 1 microg/kg i.p.)- and vasopressin (AVP, 5 microg/kg i.p.)-induced ACTH and corticosterone secretion was investigated in both non-stressed and crowded rats. The NO synthase blocker Nomega-nitro-l-arginine (l-NNA, 2 mg/kg i.p. ) significantly augmented the AVP-induced ACTH and corticosterone secretion in control and stressed rats, but it increased the CRH-induced ACTH response only in control rats. Crowding stress did not affect the l-NNA evoked increase in AVP-induced hormone responses, but it abolished the CRH-induced ACTH response.

Animals↗
PubMed1999

Blockade of nitric oxide formation impairs adrenergic-induced ACTH and corticosterone secretion.

It has been suggested that adrenergic agents might modulate the L-arginine-NO pathway. Sympathomimetic agonists enhance the basal release of NO, and noradrenaline increases the synthesis of nitric oxide synthase (NOS) in the medial basal hypothalamus in vitro. In the present study possible involvement of NO in central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic agents was investigated in conscious rats. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME 2 and 10 microg) was administered intracerebroventricularly (i.c.v.) 15 min before the adrenergic agonist given by the same route; 1 h later the rats were decapitated. Plasma levels of ACTH and corticosterone were measured. L-NAME significantly diminished the ACTH and corticosterone response to phenylephrine (30 microg), an alpha1-adrenergic receptor agonist. These hormone responses to clonidine (10 microg), an alpha2-receptor agonist, were dose-dependently suppressed or totally abolished by L-NAME. A significant rise in the ACTH and corticosterone secretion induced by isoprenaline (10 microg), a beta-adrenergic receptor agonist, was only moderately diminished by pretreatment with L-NAME. These results indicate that NOS is considerably involved in central stimulation of the HPA axis by alpha1- and alpha2-adrenergic receptor agonists, and that NO mediates the stimulatory action of these agonists on ACTH and corticosterone secretion. The stimulation induced by beta-adrenergic receptors is only moderately affected by endogenous NO.

Adrenergic Agonists↗
PubMed1998

Effect of L-NAME, a specific nitric oxide synthase inhibitor, on corticotropin-releasing hormone-elicited ACTH and corticosterone secretion.

This study was designed to determine the role of endogenous nitric oxide (NO) in the corticotropin-releasing hormone (CRH)-induced ACTH and corticosterone secretion, as well as possible involvement of hypothalamic dopamine and noradrenaline in that secretion in conscious rats. CRH given i.p. stimulated dose-dependently the pituitary-adrenocortical activity measured 1 h later. Dexamethasone (0.2 mg/kg i.p.) injected 1 h before CRH (1 microg/kg i.p.) totally abolished the CRH-elicited ACTH and corticosterone secretion, indicating a predominantly pituitary site of CRH-evoked stimulation. L-arginine (120 mg/kg i.p.) and N(omega)-nitro-L-arginine methyl ester (L-NAME 5-10 mg/kg i.p.) did not markedly affect the basal plasma ACTH and corticosterone levels. L-NAME given 15 min before CRH markedly, but not significantly, augmented the CRH-induced ACTH response, and enhanced more potently and significantly the corticosterone response. Pretreatment with L-arginine, a substrate for NOS, slightly diminished the CRH-induced ACTH response and considerably reduced the corticosterone response. L-arginine also significantly reversed the L-NAME-evoked increase in the CRH-induced ACTH and corticosterone secretion. L-NAME did not markedly alter the CRH-induced hypothalamic dopamine and noradrenaline levels, while L-arginine significantly increased noradrenaline level. However, those alterations were not directly correlated with the observed changes in ACTH and corticosterone secretion. These results indicate that in conscious rats NO plays a marked inhibitory role in the CRH-induced ACTH secretion and inhibits more potently corticosterone secretion. Hypothalamic dopamine and noradrenaline do not seem to be directly involved in the observed alterations in ACTH and corticosterone secretion.

Adrenocorticotropic Hormone↗
PubMed1998

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

In the present study the role of endogenous nitric oxide (NO) in the vasopressin-induced ACTH and corticosterone secretion was investigated in conscious rats. Vasopressin (AVP 5 microg/kg i.p.) considerably augmented ACTH and corticosterone secretion. L-arginine (120 and 300 mg/kg i.p.) did not significantly alter the AVP-induced secretion of those hormones. Nitric oxide synthase (NOS) blockers N(omega)-nitro-L-arginine (L-NNA) and its methyl ester (L-NAME) given i.p. 15 min before AVP markedly increased the AVP-induced ACTH secretion. L-NNA (2 mg/kg) more potently and significantly increased the AVP-induced ACTH secretion, whereas L-NAME elicited a weaker and not significant effect. Both those NOS antagonists intensified significantly and to a similar extent the AVP-induced corticosterone secretion. L-arginine (120 mg/kg i.p.) reversed the L-NNA-induced rise in the AVP-stimulated ACTH secretion and substantially diminished the accompanying corticosterone secretion. Neither vasopressin alone nor in combination with L-arginine and L-NAME evoked any significant alterations in the hypothalamic noradrenaline and dopamine levels. L-NNA (2 and 10 mg/kg i.p.) elicited a dose dependent and significant decrease in the hypothalamic noradrenaline level. The hypothalamic dopamine level was not significantly altered by any treatment. These results indicate that in conscious rats endogenous NO has an inhibitory influence on the AVP-induced increase in ACTH and corticosterone secretion. L-NNA is significantly more potent than L-NAME in increasing the AVP-induced ACTH secretion. This may be connected with a considerable increase by L-NNA of hypothalamic noradrenergic system activation which stimulates the pituitary-adrenal axis in addition to specific inhibition of NOS.

Adrenocorticotropic Hormone↗
PubMed1998

Effect of indomethacin on nicotine-induced ACTH and corticosterone response.

The effect of nicotine on ACTH and corticosterone secretion and possible mediation of prostaglandins in this secretion was investigated in conscious rats. Nicotine (5 and 10 mg/kg i.p.) considerably increased the plasma ACTH and corticosterone levels, measured 1h after injection. Mecamylamine (10 and 50 micrograms i.c.v.), a nicotinic receptor antagonist, given 15 min prior to nicotine dose-dependently diminished the ACTH and corticosterone responses, by 59 and 30% respectively. Pretreatment with hexamethonium (2 mg/kg i.p.), a peripheral blocker of nicotinic receptors, diminished to a similar extent the nicotine-induced ACTH and corticosterone responses. On the other hand atropine, a muscarinic receptor antagonist, did not markedly alter those responses. Systemic or intracerebroventricular pretreatment with indomethacin (2 mg/kg i.p. or 0.1 and 1 microgram i.c.v.), a cyclooxygenase and endogenous prostaglandin synthesis blocker considerably reduced, by 58%, the nicotine-induced ACTH response, but did not alter the corticosterone response. These results show that nicotine given systemically stimulates ACTH and corticosterone secretion by selective activation of central and peripheral acetylcholine nicotinic receptors. Endogenous prostaglandins are significantly involved in the nicotine-induced central stimulation of ACTH secretion. Prostaglandins do not directly affect the nicotine-induced corticosterone secretion from the adrenal cortex.

Adrenocorticotropic Hormone↗
PubMed1998

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

Involvement of the central adrenergic system in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by carbachol, a cholinergic muscarinic agonist, was assessed indirectly through corticosterone secretion. Carbachol (2 micrograms) given intracerebroventricularly or intraperitoneally evoked a dose-related increase in serum corticosterone levels. On a molar basis, carbachol given i.c.v. was considerably more active than when injected i.p., indicating its central site of action. The corticosterone response to i.c.v. carbachol was significantly reduced by pretreatment of rats 15 min earlier with prazosin, an alpha 1-adrenergic receptor antagonist. Pretreatment with yohimbine, an alpha 2-adrenergic antagonists, did not significantly affect the carbachol-induced corticosterone response. Propranolol, a beta-adrenergic blocker, given i.c.v. or i.p. significantly impaired the carbachol-elicited corticosterone secretion. The selective noradrenergic neurotoxin DSP-4 (50 mg/kg) given i.p. 8 days before the experiment, also potently diminished the carbachol-induced rise in serum corticosterone levels. Carbachol markedly increased, while DSP-4 significantly diminished the hypothalamic noradrenaline levels. Likewise, DSP-4 significantly impaired the carbachol-induced rise in hypothalamic noradrenaline levels. Our present results indicate that the central adrenergic system is involved in the cholinergic muscarinic stimulation of the pituitary-adrenocortical response. Both hypothalamic noradrenaline and adrenergic alpha 1- and beta-receptors are significantly involved in the carbachol-induced HPA response.

Adrenergic Antagonists↗
PubMed1997

Corticosterone response induced by intracerebroventricular administration of met-enkephalin and naloxone in rats under stress.

In rats exposed to a 10 min restraint stress naloxone (0.1-10 micrograms) administered intracerebroventricularly (i.c.v.) did not substantially alter the hypothalamic-pituitary-adrenal (HPA) stress response, measured indirectly through serum corticosterone levels. Met-enkephalin (10-200 micrograms i.c.v.) dose dependently increased the stress-induced corticosterone response. The increase in corticosterone secretion elicited by met-enkephalin was markedly diminished by pretreatment with naloxone. The adrenergic alpha 1- and alpha 2-receptor antagonists, prazosin and yohimbine did not significantly affect the met-enkephalin-induced increase in serum corticosterone levels in stressed rats. Conversely, propranolol, a beta-adrenergic receptor antagonist, abolished the met-enkephalin induced corticosterone response. These results indicate that opioid receptors are not significantly involved in the HPA response to a short restrains stress. In stressed rats met-enkephalin stimulates, by a central mechanism, the hypothalamo-pituitary-adrenocortical activity via opioid- and beta-adrenergic but not alpha-adrenergic receptors.

Animals↗
PubMed1997

Effect of naloxone on central adrenergic stimulation of corticosterone secretion.

The interaction of central opioid with adrenergic system in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis was investigated in conscious rats. All the tested drugs were administered intracerebroventricularly (i.c.v.), naloxone 15 min before the adrenergic agonists. Phenylephrine (30 micrograms), clonidine (10 micrograms) and isoprenaline (10 micrograms), the alpha 1-, alpha 2- and beta-adrenergic agonists as well as noradrenaline (10 micrograms) and adrenaline (10 micrograms) significantly increased the serum corticosterone levels, measured 1 h after drug administration. Naloxone (0.01-1 microgram) did not markedly influence the corticosterone response to phenylephrine and isoprenaline and diminished by a half the response to clonidine. Naloxone also significantly decreased the corticosterone response to noradrenaline but did not substantially alter the response to adrenaline. Noradrenaline potently stimulates the HPA axis via alpha 2-adrenoceptors, whereas adrenaline involves mainly alpha 1- and beta-adrenergic receptors. These results indicate that central opioid system is significantly involved in mediating the pituitary-adrenocortical response to clonidine and noradrenaline but not phenylephrine, isoprenaline and adrenaline. This suggests an interaction of opioids at central alpha 2- but not alpha 1-receptor sites.

Adrenal Cortex↗
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↗
PubMed1997

Role of nitric oxide in the vasopressin-induced corticosterone secretion in rats.

The presence of nitric oxide synthase (NOS) in hypothalamic structures which control the activity of the hypothalamic-pituitary-adrenal (HPA) axis suggests a role for NO in regulation of ACTH and corticosterone secretion. We investigated the involvement of NO in the corticosterone secretion induced by vasopressin (AVP), a potent coregulator of the HPA activity. AVP injected i.p. was, on a molar basis, considerably more potent than administered intracerebroventricularly in inducing corticosterone secretion. This finding suggests a preferential action of AVP on pituitary corticotrop receptors, but not on central structures involved in stimulation of the HPA axis. Dexamethasone given before AVP totally abolished the AVP-elicited corticosterone response by a feedback mechanism and/or inhibition of the phospholipase A2 activity and prostaglandin synthesis. Pretreatment with the NOS inhibitors L-NAME and L-NNA augmented significantly and to a similar extent the corticosterone response to AVP administered both systemically and centrally and L-NNA was found to be more potent in this respect. Pretreatment with L-arginine markedly reduced the AVP-induced corticosterone response. These results suggest that endogenous nitric oxide is significantly involved in the AVP-elicited corticosterone secretion and NO-induced alterations in the prostaglandin synthesis may participate in this action.

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↗
PubMed1996

Effect of indomethacin on the CRH- and VP-induced pituitary-adrenocortical response during social stress.

The role of prostaglandins (PGs) on the corticotropin-releasing hormone (CRH)- and vasopressin (AVP)-induced pituitary-adrenocortical response under basal and social stress circumstances was investigated. Crowding stress applied for 3 days did not diminish the CRH-elicited corticosterone response, but it considerably reduced such a response to AVP. In control rats systemic or icv pretreatment with indomethacin, an inhibitor of PGs synthesis, did not affect the corticosterone response to ip or icv CRH administered 15 min later. By contrast, ip or icv pretreatment with indomethacin considerably reduced the corticosterone response to AVP given by either route in control rats. Similarly, ip pretreatment with indomethacin further reduced the corticosterone response to AVP already diminished by crowding stress. These results indicate that hypothalamic and anterior pituitary PGs are not involved in the CRH-elicited pituitary-adrenocortical response, but they significantly mediate this response to AVP under both basal and social stress circumstances.

Adrenal Cortex↗