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PubMed1978

Some effects of adrenalectomy in the fatty rat.

Function of the pituitary-adrenal axis was examined in lean and genetically obese fatty (Zucker) rats. The diurnal rhythms of plasma corticosterone and plasma ACTH were similar in both groups. The secretion of corticosterone by adrenal glands incubated in vitro with graded doses of ACTH was also comparable in lean and fatty rats. Adrenalectomy reduced food intake and weight gain in the fatty rats to levels similar to those in the lean animals and raised plasma ACTH to the same level. The injection of corticosterone (2 and 10 mg/day) increased food intake more in adrenalectomized fatty rats than in the corresponding lean ones. Progesterone increased food intake similarly in both groups. The enhanced responsiveness to corticosterone could account for many of the metabolical defects in the fatty rat.

Adrenalectomy↗

PubMed1979

Effect of stress, adrenocorticotropin or corticosteroid treatment, adrenalectomy, or hypophysectomy on hypothalamic immunoreactive adrenocorticotropin concentrations.

Despite variations in plasma and/or pituitary ACTH concentrations, no changes in median eminence or medial basal hypothalamic immunoreactive ACTH-like concentrations were seen in rats studied 6 weeks posthypophysectomy, 12 h or 28 days after bilateral adrenalectomy, 6 days after implantation of corticosterone pellets (75 mg), after dexamethasone administration (300 micrograms/100 g BW, ip, twice daily for 4 days), or after chronic immobilization stress. The lack of concordant variation of brain, pituitary, and plasma ACTH concentrations further supports the suggestion of a nonpituitary, central nervous system origin of some portion of brain immunoreactive ACTH-like activity.

Adrenal Cortex Hormones↗

PubMed1981

Naloxone, adrenalectomy, and steroid replacement: evidence against a role for circulating beta-endorphin in food intake.

Naloxone has a dose-dependent, significant anorectic effect when administered to normal rats, consistent with an antagonism of central or peripheral enkephalinergic or endorphinergic mechanisms. Mean levels of circulating immunoreactive beta-endorphin were similar in intact rats (0.5 ng/ml) and dexamethasone-treated adrenalectomized rats (0.5 ng/ml). In contrast, plasma levels were high in adrenalectomized rats with no replacement steroid (1.3 ng/ml) and in adrenalectomized rats given the mineralocorticoid deoxycorticosterone (0.9 ng/ml). In sharp distinction to the clear changes in circulating immunoreactive beta-endorphin produced by adrenalectomy and selective steroid replacement, no differences were seen in baseline food intake or anorectic response to naloxone. We conclude that a physiological role for circulating beta-endorphin in the regulation of food intake appears unlikely.

Adrenal Cortex Hormones↗

PubMed1983

Effect of adrenalectomy on renin release in the rat.

The purpose of this study was to evaluate the mechanism of increased renin secretion in the adrenalectomized (Adx) rat. Plasma renin concentration (PRC) responses to acute infusion of 0.9% NaCl (5% of body weight) were compared in three groups of rats: Adx, Adx rats treated with dexamethasone (Adx + Dex), and sham controls. During the 7 days after adrenalectomy and before acute infusion. Adx animals drank 0.9% NaCl; sham animals drank water. Despite a more positive sodium balance over the 7 days, preinfusion PRC was higher in Adx than in the other two groups (P less than 0.01) and did not decrease with NaCl infusion [31.2 +/- 9.6 (+/-SE) U/30 min to 30.4 +/- 9.5]. PRC was suppressed by NaCl infusion in Adx + Dex (10.2 +/- 2.4 to 4.1 +/- 1.2) and sham controls (9.7 +/- 0.9 to 2.6 +/- 0.5). In separate groups of animals, PRC decreased (P less than 0.01) in response to volume expansion with 25% albumin (1% of body weight) in both Adx (42.6 +/- 8.9 to 23.1 +/- 6.1) and sham controls (10.2 +/- 1.2 to 2.1 +/- 0.7). These results are consistent with the hypothesis that altered responsiveness to NaCl, in the absence of volume contraction, contributes to increased renin release in adrenal insufficiency. Glucocorticoid replacement restored renin responsiveness to NaCl.

Adrenal Glands↗

PubMed1984

The effect of adrenocorticotropin or hydrocortisone on serum luteinizing hormone concentrations after adrenalectomy and/or ovariectomy in the prepuberal gilt.

The possible role of ACTH and the adrenal gland in modulating LH secretion in prepuberal gilts was studied. Fifty-one gilts, 170-175 days of age, were randomly assigned to 12 treatments in a 2 X 2 X 3 factorial design. The main treatments were adrenalectomy (ADX) or sham-ADX, ovariectomy (OVX) or sham-OVX, and ACTH, hydrocortisone acetate (HCA), or vehicle (V) administration. ACTH, HCA, or V was administered from days 3-10 after surgery. Beginning at 0800 h on day 10, blood samples were collected every 15 min for 16 h via jugular cannulae. At 1600 and 2000 h, all gilts were injected iv with a pharmacological dosage of 400 micrograms GnRH. ADX and OVX did not influence subsequent serum cortisol (CS) concentrations, detected by RIA. HCA elevated serum CS concentrations in all four surgical groups. ACTH treatment elevated serum CS and progesterone concentrations only in the sham-ADX groups. Every 3 days after surgery, all ADX gilts received 10 mg deoxycorticosterone acetate, im, as an electrolyte maintenance treatment, which may have been detected in the peripheral blood by the CS assay since the cross-reaction of deoxycorticosterone with the first antibody of the CS assay was 17.1%. Serum LH concentration, peak frequency, and peak magnitude were greater in V-treated OVX gilts than in V-treated sham-OVX gilts in both ADX and sham-ADX groups. Chronic ACTH treatment blocked the increase in basal serum LH concentration, peak frequency, and peak magnitude after OVX only when the adrenal glands were present. In contrast, HCA blocked the postcastration increase in the basal serum LH concentration and peak magnitude in the presence or absence of the adrenal glands. However, HCA had no effect on the increased frequency of LH peaks that occurred after OVX in V-treated gilts. The serum LH responses after both GnRH challenges were similar for all gilts, and the LH response to the second GnRH challenge was less than that observed after the first challenge. These data indicate that ACTH and HCA suppressed the postcastration increase in LH secretion. However, the effect of ACTH was mediated through the adrenal gland, and the inhibiting influence of ACTH and HCA on LH secretion was apparently not mediated at the pituitary level in the prepuberal gilt.

Adrenalectomy↗

PubMed1984

Hormonal regulation of prolactin receptors in male rat target tissues: the effect of hypothyroidism and adrenalectomy.

The effects of hypothyroidism and adrenalectomy (ADX) on PRL receptors as well as the subcellular distribution of PRL-binding sites in adult male rat target tissues were investigated. In ventral prostate, kidney, and adrenal, PRL-binding activity was enriched in the 15,000 X g pellet (mitochondrial/Golgi fraction). The zona fasiculata/reticularis plus medulla of the adrenal had higher PRL-binding activity than the zona glomerulosa (plus capsule). Propylthiouracil-induced hypothyroidism significantly decreased PRL binding to kidney (65%) and testis (50%), and 16-h replacement with T4 restored PRL binding to control levels. T4 was, however, without effect on renal PRL binding in hypothyroid castrated rats, indicating that androgen may be required for this response. The increase in PRL binding to ventral prostate and adrenal due to hypothyroidism was not reversed within 16 h of T4 injection, whereas T3 injection decreased PRL binding to ventral prostate within 12 h. ADX increased PRL binding to rat testis (38%) and kidney (18%), and 5-day replacement with dexamethasone decreased PRL binding to levels lower than those in control rats. ADX had no effect, and dexamethasone treatment decreased (16-20%) PRL binding to ventral prostate and hCG binding to rat testis. The modulation of PRL receptors by hypothyroidism and ADX suggests that thyroid and adrenal hormones play a role in the regulation of PRL receptors.

Adrenal Glands↗

PubMed1986

The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine.

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.

Adrenalectomy↗

PubMed1987

Vasopressin-containing and vasopressin-deficient subpopulations of corticotropin-releasing factor axons are differentially affected by adrenalectomy.

CRF-containing parvocellular axons in the external zone of the rat median eminence were classified as vasopressin-containing (CRF+/AVP+) and vasopressin-deficient (CRF+/AVP-) subpopulations based on post-embedding electron microscopic immunocytochemical staining of serial ultrathin sections for CRF, AVP and the other peptides derived from the AVP precursor: AVP-associated neurophysin (NP-AVP) and the C-terminal glycopeptide (GP). In normal animals, the CRF+/AVP+ and CRF+/AVP- subpopulations were approximately equal in terms of detectable axonal swellings. Three to 14 days after adrenalectomy (ADX), the CRF+/AVP+ and CRF+/AVP- subpopulations represented about 95% and 5%, respectively, of total CRF+ swellings. This change was due to a 90% decrease in the absolute number of detectable CRF+/AVP- swellings after ADX, whereas the absolute number of detectable CRF+/AVP+ swellings rose by less than 20%. These changes were completely blocked by administering the glucocorticoid agonist dexamethasone throughout the period after ADX. The results suggest that the CRF+/AVP+ and CRF+/AVP- subpopulations of neurosecretory axons in the external zone of the median eminence respond differently to ADX, indicating that they are independently regulated by glucocorticoids.

Adrenalectomy↗

PubMed1989

The development of corticotrophs in the fetal sheep pars distalis: the effect of adrenalectomy or cortisol infusion.

At 90 days gestation a uniquely fetal-type and an adult-type corticotroph have been observed in the fetal sheep pars distalis (term approximately 147 days). Between 90 and 130 days gestation the fetal type is predominant, and its numbers decline toward term. In this study the effect of the endogenous cortisol surge on the change in the population of corticotrophs in the pars distalis was investigated in sheep fetuses after bilateral adrenalectomy at 120 days gestation or after an infusion of 2 mg cortisol/day between 109 and 115 days gestation. The total proportion of corticotrophs, expressed as a percentage, decreased significantly (P less than 0.01) from 115 days in saline-infused controls (21.09 +/- 1.10%) and 135 days in intact controls (14.59 +/- 1.12%). The percentage of adult-type corticotrophs increased significantly (P less than 0.01) from 5.65 +/- 0.77 at 115 days, to 11.93 +/- 1.41 at 135 days. The percentage of fetal-type corticotrophs decreased significantly (P less than 0.001) from 14.91 +/- 0.35 at 115 days to 2.33 +/- 0.48 at 135 days. A small proportion of ACTH-immunoreactive cells could not be defined as either adult- or fetal-type corticotrophs. These changes in the corticotroph population had not occurred at 135 days in fetuses that had been adrenalectomized at 120 days; the percentage of corticotrophs relative to unstained cells (21.70 +/- 0.46%), the percentage of adult-type corticotrophs (6.42 +/- 0.29%), and the percentage of fetal-type corticotrophs (14.65 +/- 0.49%) were similar to those in 115-day-old fetuses, indicating that the normal change in the corticotroph population between 115 and 135 days gestation was dependent upon the presence of the fetal adrenal. In fetuses exposed to exogenous cortisol between 109 and 115 days gestation, the percentage of corticotrophs relative to unstained cells (16.53 +/- 1.68%), the percentage of adult-type corticotrophs (12.40 +/- 1.34%), and the percentage of fetal-type corticotrophs (3.78 +/- 0.58%) were similar to those at 135 days. This indicates that a short period of increased fetal plasma cortisol can bring about premature maturation of the corticotrophs in the fetal sheep pars distalis. We have also described an ACTH-immunoreactive cell which has characteristics of both an adult- and a fetal-type corticotroph. Its morphological appearance suggests that it may be a transitional stage from the fetal- to the adult-type corticotroph.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗

PubMed1990

Adrenalectomy in the neonate: adult-like adrenocortical system responses to both removal and replacement of corticosterone.

Neonatal rats exhibit a period of diminished responsiveness to stress between days 3-10 of life, which has been shown to be associated with an increased sensitivity to corticosterone (B) inhibitory feedback. In this study we further investigated B feedback potency on regulation of ACTH by examining 1) the time course of changes in pituitary ACTH secretion and content, plasma B and B-binding globulin (CBG) concentrations, and thymus weight after adrenalectomy (ADX) performed on 5-day-old pups, with or without sc 5% B pellet replacement, and 2) the time required for acute (B injection) and the B dose required for constant (B pellet) inhibition of ACTH secretion in 10-day-old ADX neonates. As in adult rats, ADX in neonates caused an immediate (3 h) large increase (13-fold) in plasma ACTH levels compared to that in sham-operated rats, followed by a decrease by 12 and 24 h after surgery and a further and sustained increase during the next 4 days. Pituitary ACTH stores were diminished in ADX rats by 3, 12, and 24 h and increased thereafter. Five percent B pellet replacement abolished ADX-induced changes in plasma and pituitary ACTH until days 4-5, when plasma ACTH was slowly released from B inhibition (circulating B values were similar to ADX values). By day 10 of life, inhibition of plasma ACTH by calculated free B showed an IC50 of 1.09 nM. Plasma CBG concentrations exhibited a clear developmental pattern in sham-operated rats, being lower on days 6-8 than earlier or later. Typical ADX-induced increases in CBG levels were observed from day 3 on after surgery, at the same time as a transient decrease in CBG levels occurred in ADX plus 5% B rats. On day 10 of age, inhibition of CBG by calculated free B demonstrated an IC50 of 1.5 nM. Although no enlargement of the thymus was observed after neonatal ADX, thymus weight was significantly diminished by 12 h after B replacement and in a dose-related manner at 5 days with B pellets containing 5-25% B. The thymus contained mostly type II glucocorticoid receptors, which did not up-regulate 3 h or 5 days after ADX. Acute sc injection of B (10-34 micrograms/g BW) in 10-day-old rats inhibited ADX-induced ACTH secretion within 30 min, and the estimated half-time for the inhibition was 40 min. By 2 h after B injection, plasma ACTH levels were comparable to those in sham-operated animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex↗

PubMed1975

Precocious puberty: the effect of adrenalectomy on PMS-induced ovulation and progesterone secretion.

Female Sprague-Dawley derived rats were received at 21 days of age and either sham-operated or adrenalectomized on that day. Half of the animals received either 25 IU pregnant mare's serum gonadotrophin (PMS) or 0.9 saline at 9 AM on the next day; the other half were injected at 26 days of age. On the day of expected ovulation (days 24-25 and days 28-29) the rats were killed at 4-hr intervals and the incidence of ovulation determined. Serum progesterone and corticosterone were measured with the intent of comparing the pattern of these steroids with the timing and incidence of ovulation. Twenty-two-day-old rats given PMS ovulated later (at 0400 on day 25) than did the 26-day-old rats (at 2400 on day 28). Adrenalectomized ADRX rats ovulated later than intact controls at both ages (ovulation complete at 1600 on days 25 and 29, respectively). There was a reduced ovarian weight response to PMS in ADRX rats but uterine weights were not consistently different from intact PMS-treated rats. Associated with the different timing of ovulation and organ weight response in the ADRX rats there was a lower serum progesterone response on days 24-25. In intact PMS-treated rats, the rhythm of the serum corticosterone was different in the two age groups. It is concluded that adrenalectomy alters the normal response to PMS resulting in a delay in the time of ovulation. It is possible that the adrenal normally participates in the induction of ovulation after PMS, possibly by acting as an internal priming agent to facilitate gonadotrophin release in the young rat.

Adrenal Glands↗

PubMed1976

Studies on ACTH dynamics in cultured adenohypophyseal cells: effect of adrenalectomy or dexamethasone in vitro.

Basal or hypothalamic extract-induced ACTH or TSH secretory capacity as well as intracellular ACTH content were assessed in cultured rat adenohypophyseal cells after various pretreatments of the donor animals. Medium and intracellular ACTH or TSH were measured by radioimmunoassay. Ten-day to 2-month adrenalectomy enhanced, whereas dexamethasone pretreatment suppressed, both synthesis and secretion of ACTH in the adenohypophyseal cells. Dexamethasone may also impair the replication of the adenohypophyseal cells in vivo, as indicated by the smaller number of cells obtained per animal in the dexamethasone-treated group. No significant increase in TSH secretion was observed when adenohypophyseal cells were derived from rats fed propyl-thiouracil (PTU) for 3 weeks instead of from intact rats.

Adrenal Glands↗

PubMed1992

Adrenalectomy decreases lipocortin-I messenger ribonucleic acid and tissue protein content in rats.

Clinical and experimental observations revealed that glucocorticoid-deficient states are associated with an enhanced inflammatory response. The antiinflammatory response of pharmacological doses of glucocorticoids has been tentatively attributed to the induction of lipocortin-I. To determine whether glucocorticoid deficiency causes lipocortin-I down-regulation, the expression of lipocortin-I mRNA and protein was quantified in rats with and without adrenalectomy (ADX). The mRNA of lipocortin-I was quantified by polymerase chain reaction, using a constant amount of modified lipocortin-I cDNA transcript as an internal standard. The lipocortin-I mRNA was decreased by 56 +/- 14% in lung tissue of ADX rats. This down-regulation of lipocortin-I mRNA was not due to a nonspecific effect of ADX, since the mRNA levels of other proteins (c-fos, c-myc, c-erbA beta, and metallothionein-II) remained unchanged. The decrease in lipocortin-I mRNA in ADX rats was reflected by a corresponding decrease in tissue (lung, spleen, liver, and kidney) lipocortin-I protein content, as assessed by quantitative Western blot analysis. Thus, ADX causes a decline in lipocortin-I message and protein, an observation compatible with the increased susceptibility to inflammatory reactions in glucocorticoid deficiency.

Adrenalectomy↗

PubMed1993

Adrenalectomy augments in vivo release of norepinephrine in the paraventricular nucleus during immobilization stress.

Adrenalectomy (ADX) activates CRH neurons in the paraventricular nucleus (PVN) of the hypothalamus and increases hypothalamic norepinephrine (NE) turnover in vitro. Immobilization (IMMO) markedly increases the release of NE into extracellular fluid in the PVN. The present study assessed whether ADX affects the release of NE in the PVN in vivo in conscious rats at baseline and during IMMO and whether cortisol (CORT) treatment attenuates the effects of ADX. Concentrations of NE, the NE metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol, and the dopamine metabolite dihydroxyphenylacetic acid were measured in microdialysate samples beginning 24 h after implantation of a microdialysis probe in the PVN. Seven to 10 days after ADX or ADX plus CORT (20 mg/kg.day via osmotic minipump), animals underwent IMMO for 2 h. Adrenalectomized rats had slightly higher baseline microdialysate NE, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, and dihydroxyphenylacetic acid levels and much larger IMMO-induced responses of these compounds than did sham-operated rats. CORT treatment abolished the ADX-induced augmentation of these responses. The results indicate that ADX, by removing endogenous glucocorticoids, augments IMMO-induced release and turnover of NE and amplifies the responses of catecholamine synthesis. Glucocorticoids, therefore, appear to exert feedback inhibition on stress-induced increments in the release of NE and catecholamine biosynthesis in the PVN.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Effects of nephrectomy and adrenalectomy on the renin-angiotensin system of transgenic rats TGR(mRen2)27.

The transgenic rat TGR(mRen2) develops severe hypertension with high renin activity in the adrenal and low renin activity in the kidney. To clarify the role of the adrenal gland as a source of circulating renin in TGR rats, we investigated the effects of nephrectomy (NEPEX) and adrenalectomy (ADX) on the adrenal and plasma renin-angiotensin system. TGR rats had a high basal plasma renin concentration (PRC; 18.2 +/- 1.0 ng angiotensin-I (AngI)/ml.h) compared with Harlan Sprague-Dawley (SD) rats (7.4 +/- 0.5 ng AngI/ml.h; P < 0.01) and SD rats of the Hannover strain from which the TGR rat was derived (5.3 +/- 0.6 ng AngI/ml.h, P < 0.01); TGR rats also had high adrenal renin (83.3 +/- 8.9) compared with Harlan SD rats (5.5 +/- 0.7; P < 0.01) and Hanover SD rats (6.1 +/- 0.6 ng AngI/ml.h). NEPEX markedly increased PRC (82.4 +/- 18.8 ng AngI/ml.h, P < 0.01) and adrenal renin levels (386.3 +/- 43.9 ng AngI/adrenal.h; P < 0.01) in TGR rats. ADX significantly lowered control levels of PRC and plasma AngII in the TGR rats (19.0 +/- 1.2 to 7.7 +/- 1.2 ng AngI/ml.h and 33.5 +/- 5.6 to 12.8 +/- 2.1 pg/ml, respectively) and suppressed the increases in PRC (119.4 +/- 20.2 to 61.8 +/- 4.0 ng AngI/ml.h) and plasma AngII (95.8 +/- 9.8 to 55.1 +/- 4.3 pg/ml; P < 0.01) caused by NEPEX in TGR rats. However, the levels of PRC and plasma AngII remained high after NEPEX/ADX in TGR rats. Our results suggest that the adrenal gland is one of the main sources of circulating renin in the TGR rat, but other extrarenal sources of plasma renin also exist in these animals.

Adrenal Glands↗

PubMed1994

Adrenalectomy-induced alterations of calmodulin-dependent hippocampal adenylate cyclase activity: role of guanine nucleotide-binding proteins.

Ca2+/calmodulin-dependent processes are altered by manipulations of the hypothalamic-pituitary-adrenal axis. In particular, adrenalectomy (ADX) attenuates hippocampal, but not cortical, calmodulin-dependent adenylate cyclase activity measured during the active (waking) phase of rats. The involvement of calmodulin- and guanine nucleotide (G)-binding proteins in the effects of ADX on the activity of calmodulin-dependent adenylate cyclase were investigated. In hippocampal membranes, inclusion of the GTP antagonist guanosine 5'-O-(2-thiodiphosphate) (250 microM) caused pronounced inhibition of calmodulin-stimulated adenylate cyclase activity. Guanosine 5(1)-O-(2-thiodiphosphate) had much smaller effects on calmodulin-independent (basal and forskolin-stimulated) enzyme activity. Substitution of Mn2+ for Mg2+ in the assay medium increased basal and forskolin-stimulated adenylate cyclase activity, but abolished calmodulin-dependent activation of this enzyme in both hippocampal and cortical membranes. These treatments blunted ADX-induced attenuation of hippocampal adenylate cyclase. ADX, with or without corticosterone administration (40 mg/kg, sc, once daily), failed to alter either Gi alpha or Gs alpha membrane protein content in either hippocampus or cortex. The levels of major membrane calmodulin-binding proteins in hippocampus and cortex also were not significantly altered by ADX. These results confirm that hormonal and biochemical regulation of calmodulin-dependent adenylate cyclase is distinct from that of other adenylate cyclase family members. Changes in Gs alpha and Gi alpha protein content alone cannot account for the effects of ADX on this enzyme. Overall, our studies suggest that the effects of ADX on calmodulin-dependent adenylate cyclase may occur through a reduction in the absolute amount of the catalytic subunit or an alteration(s) in the efficiency of coupling between adenylate cyclase and its modulators.

Adenylyl Cyclases↗

PubMed1994

Basic fibroblast growth factor receptor in the rat adrenal cortex: effects of suramin and unilateral adrenalectomy on receptor numbers.

Previous studies have suggested that basic fibroblast growth factor (bFGF) is involved in the mediation of the compensatory adrenal growth response. These studies were undertaken to identify the bFGF receptor in the rat adrenal cortex and determine bFGF receptor levels in vivo. Initial studies using primary cultures of rat glomerulosa cells demonstrated a high affinity binding site with a Kd of 10 pM, consistent with reported values for the bFGF receptor; however, these results could not be demonstrated in capsule-glomerulosa tissue. Using autoradiography to verify the existence of bFGF receptors in vivo, heparin-insensitive [125I]bFGF-binding sites were concentrated primarily in the capsule and glomerulosa of the adrenal cortex, suggesting the presence of FGF receptors. The presence of bFGF receptors was further verified by demonstration of internalization of [125I]bFGF into cells of capsule-glomerulosa preps. This approach was used to demonstrate that suramin (a bFGF antagonist) pretreatment of rats results in bFGF receptor up-regulation in the adrenal cortex. In addition, we demonstrated a decrease in bFGF internalization in the remaining adrenal 24 h after unilateral adrenalectomy, suggesting the utilization of bFGF during the compensatory adrenal growth response. Together, these data support a role for bFGF in autocrine stimulation of the adrenal cortex and in the compensatory adrenal growth response.

Adrenal Cortex↗

PubMed1995

Pituitary adenylate cyclase-activating peptide gene expression in corticotropin-releasing factor-containing parvicellular neurons of the rat hypothalamic paraventricular nucleus is induced by colchicine, but not by adrenalectomy, acute osmotic, ether, or restraint stress.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a newly discovered neuropeptide that is present in high amounts in hypothalamic neuroendocrine neurons and potently stimulates the accumulation of cAMP within cells of the anterior pituitary. We have employed several specific antisera recognizing different parts of the PACAP precursor to elucidate the distribution of PACAP-like immunoreactivities in the hypothalamic components of the hypothalamo-pituitary-adrenocortical axis in sections obtained from normal and colchicine-treated rats. Using immunohistochemistry with avidin-biotin-coupled peroxidase as a reporter system, high numbers of PACAP-immunoreactive perikarya were found in colchicine-pretreated rats in many of the parvicellular subdivisions of the hypothalamic paraventricular nucleus (PVN). A few cells were also found in the magnocellular subdivisions of the nucleus, and a similar small population of cells was observed in the dorsolateral aspect of the supraoptic nucleus. Using indirect immunofluorescence, the relation between CRF- and PACAP-containing neurons in the various parvicellular subnuclei of the PVN was studied, and a high degree of colocalization was demonstrated in the neurons of the medial parvicellular part of PVN. To further study the functional implications of PACAP in the hypothalamo-pituitary-adrenocortical axis, we examined the expression of PACAP messenger RNA (mRNA) in the PVN in response to five different stimulatory paradigms that previously have been shown to stimulate CRF mRNA expression in the medial parvicellular part of the PVN. The stimulatory challenges of adrenalectomy, restraint stress, ip injection of hypertonic saline, ether stress, and intracerebroventricular injection of colchicine induced significant elevations of CRF mRNA expression in the medial parvicellular part of the PVN. In contrast, the expression of PACAP mRNA, which is hardly detectable within the medial parvicellular part of the PVN, was induced only by colchicine treatment (from undetectable levels to 177 +/- 21 dpm/g; mean +/- SEM), whereas PACAP mRNA remained undetectable in this region of the PVN after exposure to any of the other stimulatory paradigms. The onset of colchicine-induced PACAP mRNA expression in the PVN was rapid (3 h), and PACAP mRNA levels remained elevated throughout the 48-h observation period. Considering the different topography and connections of the parvicellular subnuclei of the PVN, the current observations suggest that PACAP present in parvicellular neurons of the PVN may act not only as a neuroendocrine transmitter/modulator in the hypothalamo-pituitary-adrenocortical axis, but also as transmitter mediating neurotransmission conveyed from the PVN to preganglionic neurons of the autonomic system.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex↗