The Effects of Naloxone, Dexamethasone, Deoxycorticosterone and 17‐hydroxyprogesterone on Blood Pressure Responses of Normal and Adrenalectomized Rats During Hypovolaemic Shock

Khalid, B. A. K.; Morat, Paden; Merican, Z.

doi:10.1111/j.1440-1681.1987.tb00964.x

Cited by 10 publications

(13 citation statements)

References 9 publications

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“…None of the ADX control rats survived the restraint stress, suggesting that although the stress response was primarily due to opioids, which could be blocked by NAL, other hormones from the adrenals, including corticosteroids, were also crucial to withstanding the stress. This finding is consistent with previous studies that found that a reduction in blood pressure in intact rats following anaesthesia, 22 immobilization stress 19 and hypovolumic stress 18 could be blocked by NAL. Naloxone could only fully exert its effect in the presence of corticosterone and peripheral opioids.…”

Section: Discussionsupporting

confidence: 93%

“…A similar pattern was found previously for rats stressed with light ether anaesthesia, in which the stress was assessed by tail blood pressure, 22 a response that can be reduced or completely blocked by NAL, suggesting that this behavioural response is also opioid mediated. The present findings support previous reports of stress responses assessed by different parameters that could be blocked by opioid antagonists, 18 , 48 suggesting that the endorphin system plays a major role in stress responses.…”

Section: Discussionsupporting

confidence: 93%

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Effects of Naloxone, Glycyrrhizic Acid, Dexamethasone and Deoxycorticosterone in Repetitive Stress

Ainsah

Nabishah

Osman³

et al. 1999

Clin Exp Pharma Physio

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1. The present study examined the effect of naloxone (NAL), glycyrrhizic acid (GCA), deoxycorticosterone (DOC) and dexamethasone (DEX) on daily repeated 2 h chronic restrained stress (RS) on the locomotor activity (LA) of rats tested in the open field arena to elucidate the possible roles of opioids, glucocorticoids and mineralocorticoids in response to stress. 2. Intact and adrenalectomized (ADX) rats were either injected with 0.1 mL of NAL (0.32 microgram/100 g BW), 2.4 mg/kg DOC or 120 micrograms/kg DEX or had 1.0 mg/mL GCA dissolved in their drinking water or normal saline (for the ADX group) dissolved in their drinking water. 3. In intact groups, treatment with NAL completely blocked the stress response and treatment with GCA, DOC and DEX partially prevented the stress response. Adaptation occurred on either days 4, 5, 6 or 7 for intact rats treated with DEX, DOC, GCA or control rats, respectively. All ADX control rats died following the first 2 h RS. Adrenalectomized rats treated with DEX or DOC adapted later compared with intact rats, while rats given either GCA or NAL were unable to block or adapt to chronic RS. 4. These findings demonstrate that the stress response is primarily mediated by endogenous opioids, in that it is blocked by NAL. Both mineralocorticoids and glucocorticoids, which can act centrally to inhibit endorphins, partially blocked the stress response. The effect of GCA in intact rats was similar to that of both DEX and DOC in intact rats. Adrenalectomized rats treated with GCA (despite their lack of endogenous corticosterone) showed a stress response that was significantly different from the other ADX groups, implying that GCA had effects independent of endogenous corticosterone.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Effects of Naloxone, Glycyrrhizic Acid, Dexamethasone and Deoxycorticosterone in Repetitive Stress

Ainsah

Nabishah

Osman³

et al. 1999

Clin Exp Pharma Physio

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“…Naloxone has no effect on the TBP of rats pretreated with GCA, DOC or DEX. Faden and Holaday (1979) and Khalid et al (1987) showed that naloxone treatment rapidly increased mean arterial pressure and pulse pressure in hypovolaemic shock animals, suggesting that endorphins may play a role in the pathophysiology of hypovolaemic shock. Gurll et al (198 1) demonstrated that naloxone improved survival and cardiovascular function in haemorrhagic shock even without volume replacement.…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid and Glycyrrhizic Acid Block Stress Induced Hypotension in Rats

Ruszymah

Nabishah

Aminuddin

et al. 1995

Clin Exp Pharma Physio

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1. The aim of this study was to investigate the effect of repeated exposure to stress on tail blood pressure (TBP) of normal as well as GCA (glycyrrhizic acid) and steroid treated rats. Male Sprague-Dawley rats (250 g) were exposed to ether vapour to achieve light anaesthesia prior to TBP recording. Rats were injected with either normal saline or naloxone prior to exposure to stress. Tail blood pressure was recorded daily for 2 weeks. 2. We found that ether stress caused a transient drop in TBP in control as well as in dexamethasone (DEX) treated rats. The stress-induced fall in blood pressure was reduced by naloxone in control rats but not in DEX treated rats. However the transient drop in TBP following stress was not seen in either GCA or deoxycorticosterone (DOC) treated rats. 3. We conclude that first, the reduction in TBP was due to the release of endogenous opioids caused by stress. Second, DOC may block the release of such endogenous opioids, preventing the drop in TBP in response to stress, while DEX did not. Third, GCA caused a similar mineralocorticoid effect on reversing stress induced hypotension.

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“…For the ADX rats, bilateral adrenalectomy was performed by the dorsal mid-line approach under light diethyl ether anaesthesia as described previously (Khalid et al, 1987), and its completeness was verified by inspection at the time of sacrifice. In another series of experiments, groups of normal rats were given the same dose of DOC for 1, 2 and 3 weeks to determine the long term effects of DOC.…”

Section: Animals and Treatmentsmentioning

confidence: 99%

Novel effects of deoxycorticosterone on testicular 11β-hydroxysteroid dehydrogenase activity and plasma testosterone levels in normal and adrenalectomized rats

Nwe¹,

Morat²,

Arazi³

et al. 2009

Exp Clin Endocrinol Diabetes

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The 11beta-hydroxysteroid dehydrogenase (11beta-HSD) protects the testis from the inhibitory effects of corticosterone on testosterone (T) production. The objectives of the present studies were to determine the effects of deoxycorticosterone (DOC) and its mechanism of actions on testicular 11beta-HSD activity and plasma T levels after 7 days of treatment. The results revealed that at the end of 7 days treatment, DOC significantly increased testicular 11beta-HSD activity and plasma T levels in normal rats. However, the time course showed that high plasma T levels lowered 11beta-HSD activity on day 14 and by 21 days both the levels normalized. In adrenalectomized (ADX) rats, only the enzyme activity increased significantly but not plasma T levels. Spironolactone, a competitive inhibitor of mineralocorticoid receptor (MR), did not change testicular 11beta-HSD activity in both normal and DOC treated rats suggesting that DOC did not act through MR in increasing 11beta-HSD activity. On the other hand, spironolactone significantly decreased plasma T levels in DOC treated rats. Progesterone (P), a competitive inhibitor of glucocorticoid receptors (GR) or corticosterone significantly suppressed testicular enzyme activity and plasma T levels in DOC treated normal rats. Carbenoxolone which is an inhibitor of 11beta-HSD activity significantly depressed testicular 11beta-HSD activity and plasma T levels in DOC treated normal rats. This paper suggests that DOC increased testicular 11beta-HSD activity through GR; whilst increase in plasma T levels required functioning adrenal glands. The testicular 11beta-HSD is one of the regulators of T levels and vice versa.

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The Effects of Naloxone, Dexamethasone, Deoxycorticosterone and 17‐hydroxyprogesterone on Blood Pressure Responses of Normal and Adrenalectomized Rats During Hypovolaemic Shock

Cited by 10 publications

References 9 publications

Effects of Naloxone, Glycyrrhizic Acid, Dexamethasone and Deoxycorticosterone in Repetitive Stress

Effects of Naloxone, Glycyrrhizic Acid, Dexamethasone and Deoxycorticosterone in Repetitive Stress

Mineralocorticoid and Glycyrrhizic Acid Block Stress Induced Hypotension in Rats

Novel effects of deoxycorticosterone on testicular 11β-hydroxysteroid dehydrogenase activity and plasma testosterone levels in normal and adrenalectomized rats

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