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PubMed1986

Effect of adrenalectomy and corticosterone on [3H]imipramine binding in rat blood platelets and brain.

The effect of adrenalectomy and administration of glucocorticoids on [3H]imipramine binding (IB) of rat blood platelets and brain was investigated. Adrenalectomy significantly increased both Kd and Bmax of IB in the blood platelets but not the brain of male Sprague-Dawley rats. Administration of corticosterone acetate, 1 mg/kg i.p. for 7 days, decreased both Kd and Bmax in the blood platelets of sham-operated rats, but only Bmax in adrenalectomized rats. Corticosterone administration also decreased Bmax in frontal cortex and hypothalamus of sham and adrenalectomized rats but had no effect on Kd. These results suggest that glucocorticoids may modulate imipramine binding.

Adrenalectomy↗
PubMed1984

The effect of hyper and hypothyroidism, hypophysectomy and adrenalectomy on phosphatidylethanolamine methyltransferase, phosphatidyldimethyl-ethanolamine methyltransferase and choline phosphotransferase of rat liver microsomes.

The effect of hyper- and hypothyroid, hypophysectomy and adrenalectomy on phosphatidylcholine biosynthetic enzymes, phosphatidylethanolamine methyltransferase, phosphatidyldimethylethanolamine methyltransferase and choline phosphotransferase of liver microsomes was measured in rats. There was a significant increase in the specific activity of phosphatidylethanolamine methyltransferase in the hyperthyroid rats. There was a significant reduction in the specific activity of phosphatidylethanolamine methyltransferase and phosphatidyldimethylethanolamine methyltransferase in the hypothyroid states. The choline phosphotransferase increased significantly in the hyperthyroid state and decreased in the hypothyroid animals. Hypophysectomy resulted in a significant increase in specific activity of choline phosphotransferase. A reduction in the specific activity of the phosphatidylethanolamine methyltransferase occurred after 28 days of hypophysectomy. Adrenalectomy resulted in a significant stimulation of the specific activity of phosphatidylethanolamine methyltransferase and choline phosphotransferase in liver microsomes.

Adrenalectomy↗
PubMed1983

Effects of adrenalectomy and in vivo administration of dexamethasone on ATP-dependent calcium accumulation by sarcoplasmic reticulum from rat heart.

ATP-dependent Ca2+ accumulation and (Mg2+ + Ca2+)ATPase activities were determined in cardiac sarcoplasmic reticulum (SR) from control, adrenalectomized and adrenalectomized-dexamethasone-treated rats. SR from adrenalectomized rats displayed significantly diminished rates (approximately 40 to 50%, P less than 0.001) of Ca2+ accumulation compared to SR from control rats. The decreased Ca2+ accumulating activity of the membranes from adrenalectomized compared to control rats could be observed at varying Ca2+ concentrations (0.5 to 11.9 microM); kinetic analysis showed that the velocity of Ca2+ transport but not the apparent affinity of the transport system for Ca2+ was altered by adrenalectomy. ATPase activities (with Mg2+ or with Mg2+ + Ca2+) of SR were not altered significantly following adrenalectomy. In vivo administration of dexamethasone to adrenalectomized rats led to a partial (75 to 80%) yet significant (P less than 0.01 to 0.05) restoration of Ca2+ accumulating activity of SR towards normal; dexamethasone-treatment caused decrease in basal (Mg2+)ATPase activity and enhancement in (Mg2+ + Ca2+)ATPase activity. When added in vitro, dexamethasone had no effect on Ca2+ accumulating and ATPase activities of SR from control or adrenalectomized rats. These findings imply an important role for glucocorticoids in the maintenance of membrane Ca2+ transport function, and therefore, normal myocardial contractility.

Adenosine Triphosphatases↗
PubMed1984

Effect of adrenalectomy and 5-hydroxytryptophan on phasic release of luteinizing hormone.

The effect of 5-hydroxytryptophan (5-HTP) on serum progesterone and the possible role of adrenal progesterone in mediating stimulation by 5-HTP of phasic release of luteinizing. hormone (LH) were investigated in estradiol benzoate (EB)-treated ovariectomized rats. LH surges were induced in long-term (at least two weeks) ovariectomized rats by two injections of EB (20 micrograms/rat, s.c.) with an interval of 72 hrs. Administration of 5-HTP (50 mg/kg, i.p.) at 1000 hr in EB-treated ovariectomized rats resulted in a four-fold increase in serum progesterone within 30 mins, and significantly stimulated the LH surge at 1600 hr. This facilitative effect of 5-HTP on serum LH, but not progesterone, was further potentiated in rats pretreated with P-chlorophenylalanine (PCPA) 72 hrs earlier. Adrenalectomy shortly before 5-HTP administration attenuated the LH surge in saline treated controls, and completely blocked the facilitative effect of 5-HTP on the afternoon surge of LH in rats pretreated with PCPA 72 hrs earlier. On the other hand, chronic adrenalectomy (for 6 days) followed by hydrocortisone (0.2 mg/rat/day) replacement not only had no effect on the LH surge in saline treated controls, but also failed to prevent 5-HTP from facilitating the LH surge in PCPA pretreated rats. On the first day of bleeding, the basal LH value at 1000 hr in sham operated controls was significantly suppressed by PCPA pretreatment 48 hrs earlier. The second dose of 5-HTP administered on the next day failed to potentiate LH surges in either sham operated or adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1987

Effect of hypophysectomy, adrenalectomy, pituitary hormone secretion and gastric acid secretion on neurotensin induced gastric protection against stress gastric lesions.

In previous studies we have established that intracisternal (i.c.) but not peripheral (intravenous) administration of neurotensin (NT), a brain and gastrointestinal tridecapeptide, totally prevents the development of gastric lesions produced by cold-restraint stress (CRS) with food-deprived rats. In this investigation, removal of the pituitary and adrenal gland, anterior pituitary hormone secretion and gastric acid secretion were evaluated independently as potential intermediates for NT's protective effect. NT (30 micrograms) produced a significant reduction of gastric lesions incidence and severity in intact and sham-operated controls. Adrenalectomy, but not hypophysectomy totally blocked the protective effect of i.c. NT. In addition, replacement therapy with s.c. prednisone (1 mg/kg) for 5 days following adrenalectomy did not restore the protective activity of central (i.c.) NT in adrenalectomized rats. A significant reduction of serum levels of TSH, PRL and GH following i.c. NT (30 micrograms) was observed after 2h of CRS. The gastrosecretory studies revealed that i.c. NT (30 micrograms) did not affect gastric acid secretion in pylorus ligated rats. However, blockade of peripheral (gut) cholinergic (muscarinic) receptors with i.p. atropine methylbromide (1 mg/kg) significantly raised gastric pH and reduced gastric acid concentration and output. In conclusion, the results of this study indicate that the acute protective effect of brain NT appears to be mediated, at least in part, by the sympathoadrenomedullary axis, and not by the pituitary gland or substances derived from the pituitary or by inhibition of gastric acid secretion.

Adrenalectomy↗
PubMed1982

Effect of adrenalectomy on tyrosine hydroxylase activity.

Bilateral adrenalectomy produced a fall in blood pressure and an increase in tyrosine hydroxylase activity in the superior cervical ganglion in the rat. The fall in blood pressure and the increase in tyrosine hydroxylase activity in the superior cervical ganglion were prevented by giving the adrenalectomized animals 0.9% saline as their only drinking fluid. The increase in tyrosine hydroxylase activity was also prevented by decentralization (severing the preganglionic fiber) of the superior cervical ganglion. These results suggest that the induction of tyrosine hydroxylase activity results from a reflexly mediated increase in nerve impulse traffic that results from the adrenalectomy-induced fall in blood pressure. Further characterization of this response showed that the glucocorticoid, dexamethasone, did not cause a further induction of enzyme in adrenalectomized rats whereas, treatment with epinephrine as well as dexamethasone, did result in an augmentation of the enzyme activity above that seen in the already induced adrenalectomized animals.

Adrenalectomy↗
PubMed1987

Adrenalectomy and the anorectic effects of benzodiazepine inverse agonists and opiate antagonists in rats fed a palatable diet.

The benzodiazepine (BZ) receptor inverse agonists, FG 7142 (1.25-10.0 mg/kg, IP) and CGS 8216 (2.5-20.0 mg/kg, IP), significantly attenuated the consumption of a palatable sweetened diet by non-deprived male rats in a 30 min test. Adrenalectomy failed to affect the reduction in food intake produced by these two drugs. Similarly, the anorectic effects of the opiate antagonists, naltrexone (0.3-3.0 mg/kg, SC) and diprenorphine (0.3-3.0 mg/kg, SC) in the same feeding paradigm were unaffected by adrenalectomy. So far as palatability-induced feeding in concerned, anorectic effects of BZ inverse agonists and opiate-antagonists appear to be adrenal-independent in the rat. The benzodiazepines, clonazepam (0.3 mg/kg, IP) and diazepam (1.0 mg/kg, IP), stimulated food consumption in both adrenalectomized and sham-operated animals.

Adrenal Glands↗
PubMed1989

No influence of adrenalectomy on measures of taste sensitivity in the rat.

The influence of adrenalectomy on the taste sensitivity and responsivity of Long-Evans rats to sodium chloride and sucrose tastants presented separately and in mixtures was examined using high precision gustometry, computer-controlled go/no-go operant procedures, and nonparametric signal detection measures. Relative to baseline levels, adrenalectomized rats' plasma corticosterone levels decreased by 328% while sodium chloride and water consumption increased by 548% and 165%, respectively. The same measures remained unchanged in sham-operated animals. Taste sensitivity and responsivity to sodium chloride and sucrose did not differ between adrenalectomized and sham-operated animals and discrimination performance remained the same between the groups as well. The present results support and extend previous findings that adrenalectomy and the resultant corticosteroid deficiency does not influence taste sensitivity or responsivity in the rat.

Adrenal Cortex↗
PubMed1992

Salt appetite induced by DOCA treatment or adrenalectomy in rats: analysis of ingestive behavior.

A detailed description of the increased intake of 0.5 M NaCl solution by rats after systemic treatment with desoxycorticosterone acetate (DOCA) or after adrenalectomy was obtained by measuring feeding and drinking activity every 6 s for 23 h. In both models of salt appetite, the induced increase in saline intake occurred mostly at night and in close temporal association with bouts of eating and water drinking rather than in isolation. Consequently, there was no significant change in the total number of ingestive episodes, despite the substantial increase in the number of saline bouts. Saline drinking was in small draughts that usually were preceded by food bouts and followed promptly by water bouts. These and other observations indicate that under standard maintenance conditions of ad lib access to food and fluids, adrenalectomy and DOCA treatment each produce a relatively weak stimulus of salt appetite, and large daily intakes accrue because the animals do not remain satiated and the appetite recurs repeatedly.

Adrenal Glands↗
PubMed1981

Multihormonal control of enzyme clusters in rat liver ontogenesis. I. Effects of adrenalectomy and gonadectomy.

The role of glucocorticosteroid hormones in the developmental formation of carbamoyl-phosphate synthase, ornithine transcarbamoylase, arginase, glutamate dehydrogenase, tyrosine aminotransferase, glucose-6-phosphatase, hexokinase and glucokinase activities in rat liver was investigated. Steroid hormone producing glands were either inactivated by hypophysectomy (before birth) or removed by adrenalectomy and/or gonadectomy (after birth). These procedures strongly depressed corticosterone levels. Furthermore, they decreased enzyme activities when performed before birth or after the second postnatal week. However, adrenalectomy at 1 week of age was less effective: the developmental increases in carbamoyl-phosphate synthase, ornithine transcarbamoylase, arginase, tyrosine aminotransferase and glucose-6-phosphatase activity persisted despite the absence of increasing levels of circulating corticosterone.

Adrenalectomy↗
PubMed1977

Debilitating interaction of adrenalectomy and intrahypothalamic implants of prostaglandin E2 upon open-field activity levels and sexual receptivity in estrogen-primed ovariectomized rats.

A group of estrogen-primed, ovariectomized rats was adrenalectomized and tested for sexual receptivity following hypothalamic implantations of PGE2. The combination of PGE2 and adrenalectomy led to severe debilitation as manifested by greatly reduced open-field activity scores and inhibition of estrogen and progesterone induced sexual receptivity. Neither exogenous progesterone nor corticosterone was able to restore these behaviors to normal levels. A mechanism involving PGE2 and adrenalectomy-induced transient ischemia was discussed as a possible cause of the debilitation.

Adrenalectomy↗
PubMed1983

Adrenalectomy potentiates drinking induced by renal artery constriction.

We have tested the hypothesis that the dipsogenic response to an increase in the circulating angiotensin level in the rat is mediated via release of catecholamines from the adrenal medulla. Increases in circulating angiotensin levels were induced by unilateral renal artery constriction in animals which were uninephrectomized and/or adrenalectomized, twenty four hours previously. The dipsogenic response to renal artery constriction was not attenuated by prior adrenalectomy--there was, in fact, a slight potentiation. Adrenalectomy also potentiated the dipsogenic response to injection of hypersomotic saline. We conclude that drinking following renal artery constriction is not mediated by release of catecholamines from the adrenal medulla.

Adrenal Medulla↗
PubMed1990

Morphometric changes of specific located vasopressin-reacting parvicellular neurons in the paraventricular nucleus of the rat after adrenalectomy.

The morphological-morphometric consequences of bilateral adrenalectomy on vasopressin-reacting neurons of the paraventricular nucleus of the rat hypothalamus were analyzed. Bilateral adrenalectomy led to a dramatic increase in the cellular area as well as the number of immunoreactive cells (when compared to those obtained in normal colchicine-treated animals) in the neurons located in the anterior, medial and periventricular parvicellular subdivisions of the paraventricular nucleus. By contrast, no changes were observed in either the dorsal or lateral parvicellular subdivisions or in any of the magnocellular subdivisions of the paraventricular nucleus.

Adrenalectomy↗
PubMed1990

Individual variations in hippocampal dentate degeneration following adrenalectomy.

Corticosterone appears to have two markedly different effects on cells of the hippocampus in rats. On one hand, elevated levels of corticosterone contribute to the degeneration of pyramidal cells. On the other hand, elimination of corticosterone by adrenalectomy may cause degeneration of dentate granule cells (Sloviter, Valiquette, Abrams, Ronk, Sollas, Paul, & Neubort, 1989). However, the latter response is variable. Low levels of corticoids from accessory adrenal tissue not consistently detectable by radioimmunoassay may provide sufficient hormone to maintain granule cell viability. We describe simple measures that predict which individual adrenalectomized rats have degeneration of the granule cell layer. Body weight gain after adrenalectomy is positively correlated with granule cell layer area at sacrifice 3 months after surgery. Also, short-term loss of body weight when saline drinking water is replaced with tap water predicts the degree of degeneration of the granule cell layer. These observations may aid further study of this striking effect of adrenal hormones on brain anatomy.

Adrenal Glands↗
PubMed1991

Insulin and glucagon secretion in swimming mice: effects of adrenalectomy and chemical sympathectomy.

Swimming-stress is known to inhibit glucose-stimulated insulin secretion and stimulate glucagon secretion. In the present study, in mice, we investigated the relative contribution of sympathetic nerves and the adrenals to these effects. Mice were pretreated either with adrenalectomy or chemical sympathectomy induced by i.v. injection of 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve terminals. Two days later, the mice were injected i.v. with either glucose (5.6 mmol/kg) or saline, immediately before being subjected to 2 min swimming-stress or 2 min resting. Directly thereafter, blood was sampled. In normal controls, swimming inhibited glucose-stimulated insulin secretion and elevated plasma glucagon levels (P less than 0.01). Both these responses were absent both in adrenalectomized and in chemically sympathectomized mice. We also found that in resting animals, adrenalectomy reduced plasma levels of glucagon (P less than 0.05) and glucose (P less than 0.01), and that in adrenalectomized mice, swimming lowered basal plasma insulin levels (P less than 0.05). Furthermore, 6-OHDA-treatment elevated basal plasma glucagon levels (P less than 0.01). Thus, we show that, in the mouse, the inhibition of glucose-stimulated insulin secretion and the stimulation of glucagon secretion that occur during swimming-stress are both dependent on mechanisms requiring both the adrenals and intact sympathetic nerve terminals.

Adrenalectomy↗
PubMed1994

Effects of adrenalectomy and type I or type II glucocorticoid receptor activation on AVP and CRH mRNA in the rat hypothalamus.

The brain contains two types of adrenal steroid receptors, which play a role in mediating adrenal steroid effects on neuropeptide and other types of gene expression in discrete brain regions. Because the paraventricular nuclei of the hypothalamus (PVN) have adrenal steroid-sensitive neuropeptide systems, they provide a bench-mark to assess the doses of receptor agonists that may act selectively via Type I and Type II receptors. In the present study, in situ hybridization histochemistry was used to examine the effects of adrenalectomy (ADX) and Type I and Type II receptor agonists on arginine vasopressin (AVP) mRNA and corticotropin-releasing hormone (CRH) mRNA in rat brain. In agreement with previous reports, adrenal steroid regulation of AVP and CRH mRNA was found to be mediated primarily through the Type II receptor. Furthermore, adrenalectomy significantly increased AVP mRNA in the parvocellular region of the hypothalamic paraventricular nucleus (PVN), and systemic administration of the specific Type II agonist, RU28362 (10 micrograms/microliters/h), as well as corticosterone (CORT) pellets of 50 and 300 mg, prevented this increase. CRH mRNA was not significantly increased after ADX, but was markedly decreased in the PVN of rats receiving either RU28362 or a 300 mg pellet of CORT. Aldosterone, a specific Type I agonist, did not significantly affect either AVP or CRH mRNA levels when administered at 10 micrograms/h. Moreover, in the magnocellular regions of the PVN and SON AVP mRNA did not vary as a function of steroid manipulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1995

Adrenalectomy reduces FGF-1 and FGF-2 gene expression in specific rat brain regions and differently affects their induction by seizures.

We have previously reported that limbic seizures regulate the gene expression of fibroblast growth factor-2 (basic, FGF-2) according to a specific spatio-temporal pattern. In the present paper we have investigated the role of adrenal hormones on seizure-induced elevation of fibroblast growth factor-1 (acidic, FGF-1) and FGF-2 gene expression. Adrenalectomy reduces FGF-2 mRNA expression in specific brain regions, such as frontal cortex, hippocampus and striatum, whereas FGF-1 mRNA levels were decreased only in the frontal cortex. The injection of kainic acid in adrenalectomized rats produced a widespread increase of FGF-2 mRNA with a pattern similar to sham animals as indicated by in situ hybridization. In contrast, although kainate-induced elevation of FGF-1 mRNA in the hippocampus was not influenced by adrenalectomy, its induction in frontal cortex was prevented by this surgery procedure. Taken together, these data indicate that adrenal hormones play a role in the regulation of the gene expression for fibroblast growth factors, but different mechanisms are operative in their induction following seizure activity.

Adrenal Glands↗
PubMedDate not supplied

Hypothalamic CRF-like immunoreactivity in the rat after hypophysectomy or adrenalectomy.

Hypothalamic CRF-like immunoreactivity was measured in normal, hypophysectomized or adrenalectomized adult male rats. As expected, adrenalectomy resulted in decreased levels in plasma corticosterone and increased plasma levels of ACTH; hypophysectomy resulted in decreased levels in both corticosterone and ACTH. The hypothalamic content of CRF-like immunoreactivity in animals two weeks post-hypophysectomy or adrenalectomy was approximately seven times greater than that found in intact animals. At one week, post-surgery, small but statistically significant decreases in content of CRF-like immunoreactivity were observed. The results at one week are consistent with removal of feedback effects of ACTH and corticosterone causing increased release of CRF and decreased content. The increase in CRF-like immunoreactivity two weeks post-surgery is probably not related to direct feedback effects on release but may be due to increased synthesis secondary to long term removal of feedback inhibition.

Adrenalectomy↗