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PubMed1989

The effects of adrenalectomy, corticotropin releasing factor and vasopressin on the sympathetic firing rate of nerves to interscapular brown adipose tissue in the Zucker rat.

The firing rate of the sympathetic efferent nerves to interscapular brown adipose tissue (IBAT) is lower in the obese rat compared with the lean rat. The present experiments show that adrenalectomy has no effect on nerve firing rate in the lean rat and a small but statistically nonsignificant effect in the obese rat. Injection of corticotropin releasing factor (CRF) into the IIIrd ventricle produced a dose dependent increase in the firing rate of the sympathetic nerves to interscapular brown adipose tissue (IBAT) in both lean and obese rats. The basal (unstimulated) level of firing was lower in the obese rat compared with the lean rat and remained significantly below lean values at each dose. The minimum dose of CRF to see an effect (125 ng) and the dose at which maximum effect on nerve firing rate was observed (500 ng) was similar in both genotypes. Injection of adrenocorticotropic hormone (ACTH) had no effect on nerve firing rate to IBAT. Central administration of vasopressin produced a significant increase in sympathetic firing rate to IBAT in both lean and obese rats. The temperature of IBAT was also significantly increased with vasopressin and the duration of the response was longer compared with CRF, but the minimum dose to see an effect was higher (2.5 micrograms). The response to vasopressin was greater in the obese rat compared with the lean rat but the maximum firing rate did not achieve levels observed in lean rats. Chronic infusion of CRF into the IIIrd ventricle of obese rats resulted in a reduction of food intake and body weight gain but IBAT mitochondrial GDP binding was unaltered by the treatment. These data are consistent with the hypothesis that the defect in the obese Zucker rat may be due to a glucocorticoid inhibition of CRF and/or vasopressin action in the CNS.

Adipose Tissue, Brown↗
PubMed1992

Effects of adrenalectomy and deprivation condition on food intake after phenylpropanolamine or clonidine.

alpha-Adrenergic receptors within the paraventricular hypothalamus (PVN) modulate feeding such that activation of alpha 2-adrenoceptors by drugs such as clonidine (CLON) increase feeding; whereas activation of alpha 1-adrenoceptors by drugs such as phenylpropanolamine (PPA) suppress feeding. Prior studies suggest that the feeding-stimulatory effect of alpha 2-adrenergic activation is a function of drug dose as well as the deprivation condition and adrenal status of the animal. Specifically, CLON's effects on feeding are greatest at low doses in food-satiated adrenally intact rats. Whether a similar profile is produced by alpha 1-adrenoceptor agonists such as PPA has not previously been explored. Thus, the present study provides a comparison of the effects on food intake of drug dose, deprivation condition, and adrenalectomy induced by these alpha 2- and alpha 1-adrenergic drugs. Accordingly, both adrenalectomized (ADX) as well as sham-control (SHAM) adult male rats underwent a series of 1-h feeding tests following administration of PPA (5, 10, 20 mg/kg, IP) as well as CLON (0.0125, 0.025, 0.05, 0.1 mg/kg, IP) under both deprived and nondeprived testing conditions. The results suggest that the deprivation condition, but not the surgical condition (ADX vs. SHAM), exerts the greatest overall effect on food intake following administration of alpha-adrenergic drugs.

Adrenalectomy↗
PubMed1995

An evaluation of the use of total body electrical conductivity for the estimation of body composition in adult rats: effect of dietary obesity and adrenalectomy.

Total body electrical conductance (TOBEC) has been recommended for serial measurements of body composition in animals and humans. This study examined the accuracy of the TOBEC technique in predicting body composition of a population of adult male rats that had undergone seven different treatments, including adrenalectomy and blocking of glucocorticoid receptors, in the study of the etiology of obesity. The predicted body composition values of the animals (n = 57, body weight 550 +/- 8 g) obtained by using the manufacturer's and Baer's equations were compared to the actual body composition obtained by direct carcass analysis. Both equations underestimated lean body mass and reciprocally overestimated body fat (manufacturer's 103 +/- 4 g, Baer's 55 +/- 3 g). A new prediction equation was developed based on the conductivity index and the actual lean body mass. This revised equation was able to accurately estimate the lean body mass of the animals used in the same experiment but over-estimated lean body mass of larger animals (n = 10, wt. 647 +/- 13 g). Conclusions based on multiple comparisons (Duncan's) of predicted and actual values resulted in different effects of treatments on body composition. To improve accuracy and reliability of the TOBEC technique, a prediction equation should be developed from the same population as the studied population, and experimental group sizes used for examining treatment effects should be relatively large.

Adipose Tissue↗
PubMed1978

Progesterone receptor in the rat anterior pituitary: effect of estrogen priming and adrenalectomy.

The present study was done to determine if a progesterone receptor is present in rat pituitary. Cytosol was labeled with 3H-progesterone (3HP) or 3H-R5020 (3HR) and subjected to sucrose-glycerol density-gradient centrifugation. Serum progesterone was measured for correlation with progesterone receptor levels. Two 3HP-binding peaks (4S + 6S) were evident in uterine and pituitary cytosols. The 4S peak was eliminated by competition with unlabeled cortisol leaving a single 6S peak (progesterone receptor). Estradiol (E) priming of the male or female rat increased progesterone receptor levels in pituitary cytosol as demonstrated using 3HP and 3HR, and pituitary progesterone receptor bound 3HR with a higher affinity than 3HP. Following adrenalectomy of gonadectomized rats, progesterone receptor levels were increased in pituitary and uterine cytosol of both E-primed and unprimed groups. An inverse relationship was established between serum progesterone and progesterone receptor levels in the uterus and pituitary suggesting that stress-induced adrenal progesterone secretion significantly influences progesterone receptor levels in the rat. These results demonstrate an estrogen-inducible progesterone receptor in the rat pituitary with properties similar to those of the uterine progesterone receptor.

Adrenalectomy↗
PubMed1976

Effect of adrenalectomy and dexamethasone treatment on circadian running in the rat.

Although adrenalectomy resulted in a marked decrease in total wheel running activity in male rats, the circadian rhythm of the running was not altered. Contrary to what has been previously observed in animals with intact adrenal glands, administration of the synthetic glucocorticoid dexamethasone to adrenalectomized animals resulted in an immediate increase in the amount of running with no effect on the circadian distribution of running. It was concluded that the adrenal axis had an influence on an animal's ability to express running behavior, but the adrenal axis had no influence on the neural control of the circadian rhythm of running.

Adrenal Glands↗
PubMed1990

Strain differences in adrenalectomy-induced alterations in nicotine sensitivity in the mouse.

Adult mice of four inbred strains (A, BUB, C57BL, DBA) and two selectively bred lines [Long-Sleep (LS) and Short-Sleep (SS)] were tested for differences in glucocorticoid regulation of nicotine sensitivity. One week following adrenalectomy (ADX), animals were tested for nicotine sensitivity in a battery of tests that included acoustic startle response, Y-maze activity (line crosses and rearings), heart rate and body temperature. Although each type of animal tested had increased nicotine sensitivity in at least one of the test battery measurements, there was clear evidence for a genetic influence on the scope of ADX-induced changes in sensitivity. LS animals had the largest increase in sensitivity with altered responses in four of five tests following ADX. The sensitivity of DBA animals was increased in two tests while for A, BUB, C57BL and SS animals, only one test was affected. ADX-induced alterations in nicotine sensitivity could not be explained on the basis of changes in nicotinic receptor number since changes were consistent across strains. The mechanism by which ADX causes increased nicotine sensitivity is not known. However, these data support the hypothesis that nicotine sensitivity is modulated by adrenal glucocorticoid secretion and also suggest that this phenomenon is under strict genetic control.

Adrenal Cortex↗
PubMed1990

Adrenalectomy-induced potentiation of morphine analgesia: reversal by prednisolone.

Effects of adrenalectomy (ADX) on analgesic potency and morphine (MOR) content after SC administration of 3.5 or 7 mg/kg of MOR, and effects of prednisolone (PRED) on the ADX-induced effects were studied. ADX significantly potentiated MOR analgesia at both MOR doses, and PRED reversed the ADX-induced potentiation of MOR analgesia, ADX did not affect MOR content in brain and plasma after 3.5 mg/kg MOR, but significantly increased MOR content in brain and plasma after 7 mg/kg MOR, and PRED reversed the ADX-induced increase in the MOR content. Although the analgesic potency of 3.5 mg/kg MOR in ADX group was equipotent with those of 7 mg/kg MOR in sham-operated and PRED-treated ADX groups, MOR content in the former group was significantly lower than those in the latter two groups. These results suggest that ADX potentiates MOR analgesia through both mechanisms of the increased MOR content and the increased sensitivity to MOR, and that the lack of glucocorticoids participates in both of these ADX-induced effects.

Adrenalectomy↗
PubMed1991

Adrenalectomy increases bicuculline-induced seizure sensitivity in long-sleep and short-sleep mice.

Susceptibility to bicuculline-induced seizure onset and tonus was increased in LS and SS mice after adrenalectomy (ADX). Replacement with 10% corticosterone (CCS) in ADX animals resulted in a return to seizure latencies equal to those of sham-operated (SHAM) mice. In SS mice, dexamethasone (DEX) and cholesterol-control replacement was as effective as 10% CCS in returning seizure thresholds to SHAM values. In LS mice, DEX was only effective at a low bicuculline dose. Within the sham-operated group SS mice were more susceptible to bicuculline-induced seizure onset than LS mice; however, after ADX latencies did not differ between the two lines. These results suggest that seizure thresholds are regulated to some extent by the hypothalamic-pituitary-adrenal (HPA) axis. The effects of ADX on GABA-related seizure activity may also be influenced by genotype, such that genetic differences in GABAA receptor function and adrenocortical responses in LS and SS mice may be responsible for the differential seizure latencies observed in sham-operated mice.

Adrenal Glands↗
PubMed1991

Effects of adrenalectomy on macronutrient selection patterns in the rat.

The present studies examined the effects of adrenalectomy (ADX) on nutrient selection of rats over the 24-h period, as well as during the first 2 h of the nocturnal feeding cycle. Results indicate that ADX, in rats showing generally similar preferences for carbohydrate and fat, equally suppresses intake of both of these nutrients over the 24-h period. The relative impact of ADX on carbohydrate and fat intake may shift depending upon baseline, with carbohydrate-preferring rats showing a stronger decrease in intake of this diet after ADX and fat-preferring rats exhibiting a greater decline in fat intake after ADX. Acute injections of corticosterone (CORT) and aldosterone (ALDO) are both found to restore carbohydrate as well as fat intake to ADX rats over the 24-h period. However, in the first 2 h of the dark feeding cycle, carbohydrate intake is found to be selectively suppressed after ADX, and CORT injection (0.5 and 2.0 mg/kg, SC) restores carbohydrate intake during this early dark period, while producing a small increase in fat intake only at the higher dose. This is in contrast to ALDO administration at dark onset, which has a stronger stimulatory effect on fat intake in the ADX rat but does not fully restore carbohydrate intake. These findings indicate that CORT and ALDO have differential effects on nutrient intake in ADX rats particularly at the onset of the dark cycle, and it is suggested that these effects are mediated, respectively, by the type I and type II steroid receptor systems in the brain.

Adrenal Glands↗
PubMed1993

The effects of chronic glucocorticoid excess, adrenalectomy and stress on neuropeptide Y in individual rat hypothalamic nuclei.

Several lines of evidence indicate a role for neuropeptide Y (NPY) in the modulation of the corticotroph axis. In two separate studies reported here, the concentrations of NPY and noradrenaline (NA), as well as corticotropin-releasing factor (CRF) and arginine vasopressin (AVP), were measured in extracts of individual rat hypothalamic nuclei after various manipulations producing either a state of chronic glucocorticoid excess or depletion, and also following repeated restraint stress. Alterations induced in the activity of hypothalamic neurones were inferred from the respective changes in these concentrations. 12 days after bilateral adrenalectomy (ADX), NPY levels were decreased by 24% in the arcuate nucleus (ARC) and 23% in the paraventricular nucleus (PVN, p < 0.05 vs controls). Forced immobilization of the animals for 4 h each day for 9 consecutive days (repeated stress) also decreased NPY content of the ARC by 25% (p < 0.01 vs controls), an effect blocked by the administration of glucocorticoids. NA levels in both hypothalamic nuclei were unaffected by repeated stress or ADX. Administration of glucocorticoids in the first of these studies induced decreases in NA levels by 15% and 25% in the ARC and PVN respectively (p < 0.05 vs controls). However, in subsequent experiments no significant effect of glucocorticoids on NA was observed. Our results demonstrate that the activity of the hypothalamic NPY-ergic neurones is modulated by glucocorticoids and by chronic stress. They also suggest that brainstem catecholaminergic and hypothalamic NPY-ergic neurones are differentially affected by altered glucocorticoid concentrations or by chronic stress, possibly in a stimulus-specific way.

Adrenalectomy↗
PubMed1982

Effects of adrenalectomy and glucocorticosteroid therapy on bone marrow T cells. Effect on T cell traffic and graft-versus-host (GVH) reactivity.

The effects of bilateral adrenalectomy (Ax) and glucocorticosteroid (GCS) treatment on the migratory behavior of circulating T cells in mice were evaluated by a 51Cr lymphocyte migration assay and two graft-versus-host (GVH) assays. The major new findings were that bilaterally adrenalectomizing a mouse effects it in two interrelated ways: 1) It decreases the accumulation of adoptively transferred 51Cr-labeled T cells to the bone marrow; and 2) it reduces the GVH reactivity of bone marrow cells. We also confirmed previous studies showing increases in the accumulation of T cells and increases in T cell-mediated GVH reactivity in the marrow of GCS-treated mice. We conclude that Ax has an opposite effect to that of GCS treatment on the intramarrow traffic of T cells and on T cell-mediated GVH reactivity of marrow cells.

Adrenalectomy↗
PubMed1996

Plasma catecholamine and met-enkephalin-Arg6-Phe7 responses to hypoxaemia after adrenalectomy in the fetal sheep.

We have investigated whether removal of the fetal adrenal glands alters the effect of acute hypoxaemia on the circulating concentrations of noradrenaline, adrenaline, Met-Enkephalin and Met-Enkephalin-Arg6-Phe7 (MERF) in the late gestation sheep fetus. Ewes of 6 adrenalectomized and 9 intact fetuses were subjected to a 30 min period of hypoxaemia and a 30 min period of normoxaemia between 135 and 141 days gestation. Removal of the fetal adrenals abolished the fetal adrenaline response and significantly reduced the fetal noradrenaline response to hypoxaemia. There was no significant increase in circulating Met-Enkephalin during either hypoxaemia or normoxaemia in either the intact and adrenalectomized groups. During basal conditions, plasma concentrations of MERF were significantly greater in the adrenalectomized group (1.64 +/- 0.07 ng/ml) than in the intact fetal sheep (1.04 +/- 0.05 ng/ml). There were significantly greater changes (p < 0.05) in plasma MERF concentrations during hypoxaemia than during normoxaemia in both the intact and adrenalectomized groups. Plasma concentrations of MERF were inversely correlated with arterial PO2 (r = -0.44, p < 0.01) in the adrenalectomized but not the intact group of fetal sheep during hypoxaemia. We have demonstrated therefore that the fetal adrenal is the major source of circulating catecholamines, but not Met-Enkephalin or MERF during hypoxaemia in late gestation. The increase in circulating MERF concentrations after adrenalectomy may reflect compensatory changes in the synthesis and/or secretion of MERF in developing sympathetic neurones.

Adrenalectomy↗
PubMed1985

Early adrenalectomy increases myelin content of the rat brain.

Rats were adrenalectomized (ADX) or sham-operated (SHAM) on the 11th day of life and killed on days 35-36, 63, or 151-153 for the isolation of cerebral myelin from each animal. Despite having lower overall body weights, ADX rats had heavier cerebra than SHAM control rats at all ages. Mean cerebral weight increases were 10.0% at day 35-36, 15.3% at day 63, and 16.7% at day 151-153. Recovered myelin dry weights were even more elevated in the ADX rats, but only at day 63 (41.7% increase) and 151-153 (42.1% increase). At both of these ages, there was a clear linear relationship between cerebral wet weights and the amount of myelin recovered from the cerebra. Analysis of the day-63 myelin samples showed no group differences in total cholesterol or protein concentration or in the specific activity of the myelin marker enzyme 2':3'-cyclic-nucleotide 3'-phosphodiesterase (CNP). However, myelin isolated from the ADX rats appeared to be deficient in both galactolipid and phospholipid. Optic nerve myelination was assessed in all animals by measuring CNP activity in homogenates prepared from this tissue. No difference between ADX and SHAM rats was observed at any age. These results indicate that early adrenalectomy stimulates myelin deposition in the rat brain as part of a more general, long-lasting enhancement of brain growth. Myelin from the brains of ADX animals may be slightly abnormal in its lipid composition. Finally, the optic nerve data may mean that myelination is not affected equally in all areas of the CNS by the loss of adrenal glands.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1993

Anomalous adrenalectomy-induced Fos-like immunoreactivity in the hypothalamic paraventricular nucleus of stress-hyporesponsive rats.

Cellular activity in the paraventricular nucleus of the hypothalamus (PVN) in response to adrenalectomy (ADX) and sham-ADX was measured in adult male rats, lactating females, and nursing pups using c-fos immunocytochemistry. Increased Fos-like immunoreactivity (FLI) was seen in the PVN of male rats at 4 h following ADX or sham-ADX but this increase was transient, and basal values were restored within 24 h. In suckling pups, ADX induced a marked FLI response in the PVN at 3 days and at 18 days postpartum. At 11 days postpartum, however, the FLI response was attenuated relative to adult animals, and 3- and 18-day-old pups. Similarly, in nursing mothers, ADX induced FLI at 3 days, but this response disappeared by 7 days and did not reappear by the end of the suckling period (day 21). These data indicate that c-fos expression is a sensitive indicator of hyporesponsiveness in the hypothalamic-pituitary-adrenal (HPA) system.

Adrenal Glands↗
PubMed1993

Effect of adrenalectomy and stress on interleukin-1 beta-mediated activation of hypothalamic corticotropin-releasing factor mRNA.

We have investigated the effect of (a) stress and (b) steroid feed-back on the interleukin-1 beta (IL-1 beta)-mediated increase of corticotropin-releasing factor (CRF) mRNA in the hypothalamic paraventricular nucleus. Both IL-1 beta and stress resulted in increased levels of CRF mRNA and when both were given together, the combination resulted in an additive effect on the increase in CRF transcripts. The effect of IL-1 beta was blunted by adrenalectomy, but returned when a replacement dose of dexamethasone was administered. The IL-1 beta-induced increase in CRF mRNA is dependent on the presence of circulating glucocorticoids, and its mechanism of action on CRF mRNA appears to be distinct from that activated in response to stress.

Adrenalectomy↗
PubMed1986

Compensatory increase in adrenomedullary angiotensin-converting enzyme activity (kininase II) after unilateral adrenalectomy.

Angiotensin-converting enzyme (ACE, kininase II, dipeptidyl carboxypeptidase, EC 3.4.15.1) was characterized in the adrenal medulla of male Sprague-Dawley rats. Rat adrenal medulla and lung ACE were similar in their susceptibility to Cl- activation and to the inhibition by EDTA, captopril, bacitracin and thiorphan, suggesting that rat adrenal medulla and lung ACE have similar properties. Changes in right adrenal weight and in adrenomedullary ACE activity 5 and 12 days following left unilateral adrenalectomy (UADX) were examined. Compensatory adrenocortical hypertrophy 12 days following UADX was associated with a significant increase in adrenal medullary ACE activity. This change was due not to a modified affinity of ACE for the substrate but to an alteration in ACE maximal velocity or number of available molecules. UADX had no effect on adrenocortical ACE activity. When UADX was combined with right splanchnic denervation, the increase in adrenomedullary ACE activity was blocked. The results support the existence of a functional ACE in adrenal medulla that is under neuronal control.

Adrenal Medulla↗
PubMed1992

Adrenalectomy does not change CRF secretion induced by interleukin-1 from rat perifused hypothalami.

Interleukin-1 (IL-1) is a potent hypothalamic-pituitary-adrenal (H-P-A) axis activator. The hypothalamus is considered one of the main sites of action of IL-1 on the H-P-A axis, inducing CRF secretion, which is modulated by glucocorticoids. Glucocorticoids, which modulate CRF release by a negative feedback inhibition, have been postulated to exert a permissive action on the IL-1 effect on CRF secretion. Using a continuous perifusion system of rat hypothalami, the results of the present study indicate that at the same concentrations, IL-1 beta exerted a more potent effect than IL-1 alpha stimulating CRF secretion. The increase in hypothalamic CRF release induced by IL-1 was rapidly inhibited by both dexamethasone and corticosterone. However, adrenalectomy 2 or 8 days before did not modify CRF secretion induced by IL-1 from the in vitro perifused hypothalami. These data indicate that IL-1 does not seem to induce CRF secretion by interfering with an impeding action of glucocorticoids, although the cytokine effect is negatively modulated by corticosteroids.

Adrenalectomy↗
PubMed1996

Blockade of central angiotensin II type 1 and type 2 receptors suppresses adrenalectomy-induced NaCl intake in rats.

Removal of the adrenal glands, the main site for the synthesis of aldosterone, produces an intake of sodium that is essential for survival. Using central blockade of angiotensin II (Ang II) receptors with SarIle Ang II, previous studies have shown that this intake depends on the stimulation of the brain angiotensin system. In the present study, using intracerebroventricular injection of specific antagonists of Ang II type 1 (AT1) or type 2 (AT2) receptors (losartan and PD 123319, respectively), we confirm that activation of brain angiotensin is essential for the expression of adrenalectomy-induced NaCl intake. Moreover, we show that (a) AT1 but not AT2 receptor blockade alone suppresses NaCl intake and (b) doses of AT1 and AT2 receptor antagonists that separately have no effect on NaCl intake, suppress the behavior when combined. It is proposed that AT1 receptors mediate the natriorexigenic effect of Ang II and that AT2 receptors have a permissive role on AT1 receptor stimulation.

Adrenalectomy↗