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PubMed1983

Influence of adrenalectomy and ovariectomy on gonadotrophin secretion.

In order to gain additional information on the effects exerted by adrenal hormones on gonadotrophin secretion, adult female rats have been submitted concomitantly to adrenalectomy and ovariectomy; ovariectomized animals with intact adrenals served as controls. Serum levels and pituitary concentrations of LH and FSH have been measured on post-operation days 1, 2, 7, 14 and 28. It has been found that ovariectomy, when performed alone, induces a progressive but delayed release of LH and a rapid and constant release of FSH. Ovariectomy exerts only minor effects on the concentrations of pituitary LH, while providing a strong stimulus to the intrapituitary accumulation of FSH. Adrenalectomy, superimposed on ovariectomy, advances the release of LH, and at the 4-week interval, increases serum levels of this gonadotrophin to well above those found in animals submitted only to ovariectomy; the absence of the adrenals does not significantly alter the release of FSH. Adrenalectomy, added to gonadectomy, strongly facilitates the accumulation of LH in the anterior pituitary, but decreases the resynthesis of FSH. In conclusion, these data suggest that one or more factors of adrenal origin may: (1) inhibit the release of LH without affecting the release of FSH; (2) prevent the post-gonadectomy accumulation of LH in the anterior pituitary and facilitate the re-accumulation of FSH.

Adrenalectomy↗

PubMed1986

Corticosteroid receptors in rat hippocampal sections: effect of adrenalectomy and corticosterone replacement.

Rat brain sections, located at the hippocampal level, were used to study the effect of bilateral adrenalectomy, with or without corticosterone treatment, on the number and affinity of corticosteroid binding sites. Adrenalectomy induces an increase of corticosterone receptor binding sites whereas adrenalectomy followed by in vivo corticosterone treatment produces a 50% decrease of binding site number. Increases and decreases of binding site number were not associated with a significant modification of the affinity for corticosterone. The present data show that in vivo corticosterone modulates its own number of binding sites demonstrated by in vitro binding on brain sections, in a manner which is reminiscent of changes in cytosol receptors demonstrated by conventional biochemical methods. Thus, this in vitro method provides an alternative way to study the plasticity of hippocampal glucocorticoid receptors.

Adrenalectomy↗

PubMed1984

Adrenalectomy increases norepinephrine turnover in brown adipose tissue of obese (ob/ob) mice.

The hyperphagia and rapid body weight gain normally observed in young obese (ob/ob) mice were abolished by removal of their adrenal glands, whereas food intake and weight gain of lean mice were not significantly affected by adrenalectomy. Adrenalectomy lowered body energy density (kcal/g carcass) in obese mice more than could be attributed to reduced food intake per se, suggesting that their energy expenditure was also increased. In control obese mice, low stimulation of brown adipose tissue by the sympathetic nervous system, as indicated by the low fractional rates of norepinephrine (NE) turnover in their brown adipose tissue may have contributed to the reduced energy expenditure in these animals. Adrenalectomy increased the rates of NE turnover in brown adipose tissue of obese mice to rates nearly equal to those observed in lean mice without affecting NE turnover in this tissue of lean mice. Likewise, removal of the adrenals normalized the low rates of NE turnover in hearts of obese mice without affecting lean mice. Rates of NE turnover in two other organs, white adipose tissue and pancreas, of control and adrenalectomized obese mice were similar to rates observed in lean counterparts. The adrenal may thus contribute to both the hyperphagia and the low energy expenditure by brown adipose tissue that together cause gross obesity in ob/ob mice.

Adipose Tissue, Brown↗

PubMed1984

Adrenalectomy abolishes the stress-induced increase in pituitary cyclic AMP.

We have previously demonstrated that various stressors increase pituitary cyclic AMP in vivo in the rat. In the course of studying the mechanisms mediating this response, we examined the effect of bilateral adrenalectomy on footshock-induced increases in pituitary cyclic AMP. In unoperated rats, intermittent footshock markedly increased pituitary levels of cyclic AMP and plasma levels of corticosterone and prolactin. Adrenalectomy completely abolished the stress-induced increase in pituitary cyclic AMP. The marked increase in plasma prolactin following footshock was not affected by adrenalectomy. Our results indicate that adrenal factors are involved in the stress-induced increase in pituitary cyclic AMP.

Adrenalectomy↗

PubMed1985

Subsensitive pituitary cyclic AMP response to stress following adrenalectomy is not caused by loss of adrenal epinephrine.

We have previously reported that various stressors acutely elevate levels of pituitary cyclic AMP in vivo and that this stress response is not seen in animals tested 7 or 30 days post-adrenalectomy. In this report we present data that demonstrate that the loss of the pituitary cyclic AMP stress response following adrenalectomy is not the result of the loss of stress-induced adrenal epinephrine release. These data show that (1) although administration of epinephrine to intact rats does not elevate levels of pituitary cyclic AMP, administration of epinephrine to adrenalectomized animals does not elevate pituitary cyclic AMP levels in vivo; (2) splanchnic denervation prevents stress-induced adrenal epinephrine release but does not abolish stress-induced increases in pituitary cyclic AMP; and (3) the time course of the developing subsensitive pituitary cyclic AMP response to stress following adrenalectomy is much slower (2 to 3 days) than the loss of circulating epinephrine.

Adrenalectomy↗

PubMed1984

Effects of changes in serum insulin in response to dexamethasone and adrenalectomy on insulin-sensitive phosphodiesterase in rat fat cells.

The effects of dexamethasone administration and adrenalectomy on insulin-sensitive phosphodiesterase were studied in rat fat cells. Isolated fat cells were incubated at 37 degrees C for ten minutes or without insulin. A crude microsomal fraction prepared by differential centrifugation was used for the determination of phosphodiesterase level. With dexamethasone treatment (400 micrograms/kg/day) for seven days, specific activity of the enzyme and its sensitivity (ED50) to insulin were decreased, as was the maximal responsiveness to insulin. Under conditions of adrenalectomy, the specific activity and the sensitivity (ED50) were increased while the maximal responsiveness to insulin was decreased. Following dexamethasone treatment specific insulin binding was decreased, and after adrenalectomy it increased. These findings were attributed to changes in the number of insulin receptors per cell rather than to changes in affinity. Alterations in insulin sensitivity (ED50) of the enzyme seemed to be due to alterations in insulin binding to the receptor. The reduction in maximal insulin responsiveness suggested postreceptor defects in both experimental groups. The mechanism related to alterations in the specific activity was not thoroughly clarified; however, serum insulin levels may specifically affect the enzyme activity.

Adipose Tissue↗

PubMed1985

Changes induced by corticosterone and adrenalectomy in synaptosomal and platelet uptake and binding of 5-HT. The relationship to [3H]imipramine binding.

A comparative study of the effect of adrenalectomy, treatment with corticosterone, and imipramine on platelet an synaptosomal uptake was undertaken. One day after adrenalectomy, uptake of 5-hydroxytryptamine (5-HT) in the platelet and the hypothalamus was significantly decreased with an increase in the apparent Km, but the uptake of 5-HT of the cerebral synaptosomes was unchanged. In this group, the Kd of low affinity binding of 5-HT was also increased in the hypothalamic synaptosomes and in the platelet preparations. Treatment with corticosterone (5 mg/kg, i.m.) restored the decrease in the uptake of 5-HT induced by adrenalectomy in the hypothalamic synaptosomes and in the platelets, and significantly increased the uptake of 5-HT of these fractions in sham-operated rats. The binding of 5-HT was unchanged by acute treatment with corticosterone. The effectiveness of imipramine varied with the preparation and treatment group. The IC50 of the cerebral synaptosomal preparation was greater than that of the hypothalamic synaptosomal preparation. Using this latter preparation, the IC50 for imipramine in adrenalectomised, sham-operated and corticosterone-treated rats were found to be 0.04, 0.09 and 0.25 microM, respectively. These changes in sensitivity to imipramine were not reflected in the binding of [3H]imipramine which was unchanged.

Adrenalectomy↗

PubMed1989

Effects of food restriction and adrenalectomy in rats with VMH or PVH lesions.

The effects of adrenalectomy in rats with ventromedial or paraventricular hypothalamic lesions have been studied in two experiments. Rats with ventromedial hypothalamic lesions or lesions in the paraventricular nucleus were allowed to gain weight for fourteen days at which time they were adrenalectomized. Before adrenalectomy, animals with VMH lesions ate more, gained significantly more weight than animals with lesions in the paraventricular nucleus, and both were significantly heavier and consumed more food than sham-operated controls. Following adrenalectomy, food intake decreased and both groups of lesioned animals lost weight. The animals with VMH lesions stabilized at weights above the control animals. Implantation of corticosterone enhanced weight gain and food intake in animals with lesions in either the paraventricular nucleus or the ventromedial hypothalamus. In the second experiment, one subgroup of rats with VMH lesions was adrenalectomized, and allowed to eat ad lib. Two other groups of sham-operated rats with VMH lesions served as controls. One group ate ad lib and one group was pair fed to the food intake of the adrenalectomized VMH-lesioned rats. Weight gain in the adrenalectomized VMH-lesioned rats and the pair-fed VMH-lesioned controls was similar and less than the VMH-lesioned rats eating ad lib. GDP binding to interscapular brown adipose tissue was related to the degree of weight gain, not to the presence of the VMH lesion. These data show that corticosterone is essential for the expression of obesity in both PVH- and VMH-lesioned rats. They also argue that the reduction in the activity of the sympathetic nervous system of VMH-lesioned rats as estimated by the GDP binding to mitochondria from brown adipose tissue is associated with hyperphagia.

Adipose Tissue, Brown↗

PubMed1978

Glucosamine incorporation into rat cerebrum: effect of adrenalectomy, corticosterone, exercise, and training.

Incorporation of D-[I-14C]glucosamine into various metabolic fractions was studied in an experiment designed to quantify the relative influence of physiological and behavioral factors. Different physiological states were established by sham operation (S), adrenalectomy (A), and adrenalectomy plus corticosterone replacement (H). Within each physiological condition the behavioral state was varied by swim-escape training (E), swimming exercise (X) or nonswimming controls (C). Adrenalectomy caused a generalized increase in label uptake by cerebral cortex and hippocampus, but precursor levels in the blood were elevated also, suggesting a systemic physiological effect. Behavioral state had no effect on overall uptake, but did influence the distribution of label between soluble and membrane-bound glycoproteins. These results indicate that D-[I-14C]glucosamine is an effective glycoprotein and ganglioside precursor in behavioral experiments, provided corrections for the influence of systemic physiological factors are made.

Adrenalectomy↗

PubMed1993

Adrenalectomy reduces atrial natriuretic peptide stimulated guanylate cyclase activity in rat paraventricular nucleus.

Atrial natriuretic peptide (ANP) or an Atriopeptin III analog (PL 058) stimulated cGMP formation in the membrane fraction of rat olfactory bulb, median eminence and paraventricular nucleus, in a dose-dependent manner. The effect of the Atriopeptin III analog was 20-40% greater than that of ANP. Bilateral adrenalectomy, with or without mineralo- or glucocorticoid-replacement, on ANP-stimulated cGMP formation was investigated in rat paraventricular nucleus. 11 days after bilateral adrenalectomy a reduced responsiveness to ANP- or PL 058-induced cGMP production was observed. This effect was prevented by deoxycorticosterone, but not by dexamethasone administration. Our results further support the presence of guanylate cyclase-coupled ANP receptors in brain localized target sites; and they provide evidence suggesting that guanylate cyclase-linked ANP binding sites in the PVN are susceptible to regulatory changes after adrenalectomy-induced activation of the hypothalamus-hypophyso-adrenocortical system.

Adrenal Glands↗

PubMed1984

Effect of adrenalectomy on cellular calcium metabolism and on the response to adrenergic stimulation of hepatocytes isolated from male and female rats.

The effects of adrenalectomy on cell calcium metabolism and on the effects of epinephrine on cAMP, phosphorylase a activity, and calcium efflux were studied in hepatocytes isolated from adult male and female rats. Adrenalectomy increased the total calcium of hepatocytes, all exchangeable calcium pools, and all calcium fluxes between the cellular pools in both sexes. After adrenalectomy, basal cAMP was elevated, phosphorylase a + b was decreased, but basal phosphorylase a activity was not changed. In adrenalectomized males and at all concentrations of epinephrine studied (1.10(-8)-1.10(-5)M) stimulation of calcium efflux was decreased and cAMP accumulation was enhanced, while the resulting phosphorylase a activation was depressed. In hepatocytes from adrenalectomized females there was a similar increase in cAMP accumulation induced by epinephrine, and a decrease in the stimulation of calcium efflux; however, the depression in phosphorylase a activation was much less and was significant only at 1.8(-8) and 1.10(-5)M epinephrine. In the male, while activation of phosphorylase a shifted from a pure alpha-adrenergic response mediated by calcium to one also involving a cAMP-mediated beta-adrenergic response, the contribution of the attenuated calcium signal was still significant. Hepatocytes from female rats did not show a comparable alpha- to beta-shift, since the relative contribution of calcium and cAMP to phosphorylase activation was similar in sham-operated and adrenalectomized animals.

Adrenalectomy↗

PubMed1992

Na(+)-Ca2+ antiporter activity of rat hepatocytes. Effect of adrenalectomy on Ca2+ uptake and release from plasma membrane vesicles.

The presence and mode of Na(+)-Ca2+ antiporter activity were studied in hepatocytes isolated from sham-operated or adrenalectomized rats and in inside-out plasma membrane vesicles isolated from rat liver. Decreasing extracellular Na+ (Na+o) immediately increased cytosolic free calcium (Ca2+i). The rise in Ca2+i was proportional to the reduction in Na+o and was caused by an increased calcium influx, presumably on the Na(+)-Ca2+ antiporter operating in the reverse mode. Perfusing the cells with Ca(2+)-free media stimulated Ca2+ efflux and decreased Ca2+i, an effect dependent on Na+o. This suggests an activation of the forward mode of Na(+)-Ca2+ exchange. There was little difference in these parameters between sham and adx groups. In contrast, steady-state calcium uptake by inside-out plasma membrane vesicles was inhibited 40% after adrenalectomy. The decreased calcium uptake was not caused by a deficiency in the ATP-dependent Ca2+ pump, whose Km and Vmax were unaffected by adrenalectomy, but by an Na(+)-dependent leak from the vesicles. Ca2+ efflux was proportional to the extravesicular Na+ concentration, suggesting that the calcium leak may take place on a Na(+)-Ca2+ antiporter. This Na(+)-dependent calcium efflux was significantly increased in vesicles prepared from adx rat livers. These results suggest that hepatocytes have functional Na(+)-Ca2+ antiporters that can operate in both forward and reverse modes. Under normal conditions, the Na(+)-Ca2+ antiporter apparently operates in the reverse mode as a Ca2+ influx pathway. The increase in Na(+)-dependent Ca2+ efflux evoked by adrenalectomy in plasma membrane vesicles could explain the recent results we obtained in hepatocytes isolated from adx rats, showing increased calcium influx, increased Ca2+i, increased intracellular calcium sequestration, and increased plasmalemmal calcium cycling.

Adrenalectomy↗

PubMed1996

Adrenalectomy enhances pro-inflammatory cytokines gene expression, in the spleen, pituitary and brain of mice in response to lipopolysaccharide.

To assess the possible influence of endogenous glucocorticoids on cytokine expression in the brain, adrenalectomized mice and sham operated mice were injected with saline or lipopolysaccharide (LPS, 10 micrograms/mouse, subcutaneously) and the levels of transcripts for IL-1 alpha, IL-1 beta, IL-1ra, IL-6 and tumor necrosis factor-alpha (TNF alpha) were determined 2 h after treatment in the spleen, pituitary, hypothalamus, hippocampus and striatum, using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Levels of IL-1 beta were measured by ELISA in plasma and tissues of mice sacrificed after the administration of LPS or saline. LPS induced the expression of pro-inflammatory cytokines at the mRNA level in all tissues under investigation, except for TNF alpha in the hippocampus. This effect was potentiated by adrenalectomy in the spleen for IL-1 alpha and IL-1ra, the pituitary for cytokines other than IL-1ra, the hypothalamus for all cytokines, the hippocampus for cytokines other than TNF alpha, and the striatum for IL-1 alpha and IL-6. In saline-treated mice, adrenalectomy increased IL-1 alpha and IL-1 beta gene expression in the hypothalamus and IL-1 alpha gene expression in the hippocampus and striatum. LPS increased plasma and tissue levels of IL-1 beta, as determined by ELISA, and this effect was potentiated by adrenalectomy in plasma and tissues other than the spleen. These results can be interpreted to suggest that endogenous glucocorticoids regulate the neural components of the host response to infection and inflammation by inhibiting cytokine expression in peripheral organs and the brain.

Adrenal Glands↗

PubMed1991

Adrenalectomy and dexamethasone administration: effect on atrial natriuretic peptide synthesis and circulating forms.

Previous in vivo and in vitro studies have reported a variety of glucocorticoid effects on the synthesis and secretion of immunoreactive atrial natriuretic peptide (ir-ANP) into plasma. To further define glucocorticoid modulation of ir-ANP, we have measured ir-ANP levels in plasma and the four cardiac chambers, and tissue ANP mRNA levels, in intact rats and adrenalectomized rats with or without dexamethasone treatment for 1, 2, 4, 8 and 16 days. Plasma levels fell by 50% between 8 and 16 days post-adrenalectomy; in contrast, dexamethasone treatment caused a 3-fold rise in plasma ANP 1-2 days post-adrenalectomy, with levels gradually returning to control by day 16. Circulating forms of ANP were unchanged by adrenalectomy or dexamethasone treatment, as were atrial ANP concentrations and ANP mRNA levels. Left ventricular ANP concentrations rose with dexamethasone treatment, and ventricular ANP mRNA levels changed in parallel with those of circulating ANP. The in vivo effect of glucocorticoids (at moderate rather than very high doses) on ANP synthesis and secretion thus appears to be predominantly but not exclusively upon the left ventricle rather than the atria.

Adrenalectomy↗

PubMed1994

Adrenalectomy alters discrete galanin mRNA levels in the hypothalamus and mesencephalon of the rat.

Using solution and in situ hybridization techniques we have studied the effects of adrenalectomy with or without restitution therapy with corticosterone on galanin mRNA levels in discrete regions of the male rat brain. Galanin peptide levels were also measured using a radioimmunoassay. The solution hybridization showed a two-fold increase in galanin mRNA 7 days, but not 14 days, after adrenalectomy in the preoptic area including the hypothalamic paraventricular nucleus (PVN). No changes were observed in the mediobasal hypothalamus including the arcuate nucleus. In situ hybridization showed that the increase in galanin mRNA was localized to the PVN and that the arcuate nucleus was not affected. The changes observed could be fully counteracted by corticosterone treatment. Radioimmunoassay showed decreased galanin levels in the median eminence 14 days, but not 7 days, after adrenalectomy and increased levels in the anterior pituitary and neurointermediate lobe. The results give evidence for a regional regulation of galanin gene expression and galanin peptide synthesis by adrenocortical steroids.

Adrenalectomy↗

PubMed1995

Behavioural deficits in adult rats following long-term adrenalectomy.

Long-term adrenalectomy results in loss of neurones in the hippocampal formation of the adult rat. The effects of long-term adrenalectomy on spatial learning and exploratory behaviour in adrenalectomized (ADX), adrenalectomized normal weight gain (ADXNW), sham operated and naive control male Sprague-Dawley rats were investigated in this study. The ADX rats had significantly longer latencies in the Morris maze task compared to the other groups. In the open-field situation, as a novel finding, the ADX rats showed significantly lower rearing scores compared to other groups. These data indicate that long-term adrenalectomy causes impairment in spatial learning and explorative behaviour in the rat.

Adrenalectomy↗

PubMed1986

Glucose and ketone bodies production in hepatocytes isolated from fetuses at term--II. Effect of maternal adrenalectomy.

Glucose and ketone bodies production has been studied in hepatocytes isolated from fetuses at term of fed and fasted adrenalectomized mothers. Maternal adrenalectomy diminishes the fetal liver weight. This effect is increased when the adrenalectomized pregnant rat is fasted for the last 2 days of gestation. Maternal adrenalectomy diminishes glucose production in hepatocytes isolated from fetuses at term. This diminution is markedly greater when the adrenalectomized pregnant rat is fasted for the last 48 hr of gestation. Maternal adrenalectomy diminishes ketone bodies production in hepatocytes isolated from fetuses at term.

Adrenalectomy↗

PubMed1992

Neurochemical changes of long-term adrenalectomy in rat brain: effects on neurotransmitter amino acids.

The levels of five amino acids together with glutamine synthetase activity, were measured in brain regions of rats with bilateral adrenalectomy, performed in newly weaning rats on postnatal day 22 and sacrificed 3 months later. Adrenalectomy caused a general decrease of glutamine concentration in three hippocampal regions (CA1-CA2, CA3, CA4-dentate gyrus), in hypothalamus, striatum and cerebellum. This reduction, which was particularly significant in hippocampus and cerebellum, was paralleled by a decrease of glutamine synthetase activity. Treatment with corticosterone reversed the effect of adrenalectomy. Little or no change was observed in the tissue levels of taurine, aspartic, glutamic or gamma-amino butyric acids.

Adrenalectomy↗