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Beta-nerve growth factor (beta-NGF) mRNA expression in the parkinsonian adrenal gland.

The adrenal gland is a well-demonstrated source for different neurotrophic factors. The presence of the beta-nerve growth factor (beta-NGF) mRNA in the adrenal tissue used for grafting in a Parkinsonian patient is reported here. Adrenal samples were obtained on the day of implantation, and a specific cDNA was synthesized after the extraction of total RNA using a synthetic oligonucleotide as a reverse transcription primer. A 168-bp portion of the cDNA was amplified using two other oligonucleotides as Taq polymerase primers in a polymerase chain reaction. Thirty-two cycles of amplification were performed. The amplification products were identified by agarose gel electrophoresis and Southern blot analysis as a single DNA band hybridizing with a third beta-NGF specific oligonucleotide. The identity of the fragment was confirmed by DNA sequencing. Quantitative analysis demonstrated a beta-NGF mRNA concentration exceeding 5 fg/micrograms of total adrenal RNA. These findings add NGF to the other neurotrophic factors produced by the gland (i.e., basic fibroblast growth factor) and demonstrate the retained functional capacity of the Parkinsonian adrenal to express the beta-NGF mRNA. All these data may assume relevant meaning for neurotransplantation research.

Adrenal Glands↗

[Adrenal gland disorders].

Adrenal diseases are generally rare but of variable manifestation and high diagnostic expenditure for definitive conformation of the disease in the individual case; therefore, the definitive diagnosis is often made by the specialist. On the other hand the supposed diagnosis, based on the knowledge of clinical symptoms, is frequently made by the nonspecialist who also initiates the first diagnostic steps in order to confirm or exclude the diagnosis. It is the aim of this survey to discuss not only the clinical symptoms of the most important adrenal diseases, but also the essential diagnostic steps in order to at least narrow down the diagnosis with as little expenditure as possible and to avoid a diagnostic maze.

Adrenal Cortex Function Tests↗

Blood supply of the ovine adrenal gland and its relevance in adrenal autotransplantation.

The arterial supply and venous drainage of 62 left and 5 right ovine adrenal glands is described, and the contribution of individual arteries to successful adrenal gland autotransplantation was evaluated. Arterial flow was measured by direct collection from the draining adrenal vein. Assessment of function of the transplanted adrenal gland was made from survival of the sheep and by the cortisol response to infusion of ACTH and the aldosterone secretory response to infusion of angiotensin II or potassium. For the left adrenal, the principal arterial supply was from the renal artery in 21 (34%), a lumbar artery in 32 (52%), and the anterior mesenteric artery in 3. The total blood flow was 5.0 +/- SEM 0.4 mL/min, the flow from the renal branch 2.3 +/- 0.3 mL/min, and the principal lumbar branch 2.6 +/- 0.3 mL/min. Venous drainage from the left adrenal was via a major adrenal vein to the left renal vein, but additional tributaries to the renal vein were present in 26%. The arterial supply to the adrenal is regional and omission of a branch at transplantation could result in infarction of portion of the gland. By defining arterial supply and measuring blood flow, selection of the appropriate artery or multiple arteries can achieve an adrenal gland autotransplant survival of 90%.

Adrenal Glands↗

Actions of somatostatin on perfused bovine adrenal glands and cultured bovine adrenal medullary cells.

The effects of somatostatin on catecholamine secretion and inositol phosphate accumulation have been studied using isolated perfused bovine adrenal glands and cultured bovine adrenal medullary cells. Somatostatin had no effect on basal adrenaline or noradrenaline secretion from either preparation. At concentrations above 1 microM, somatostatin inhibited the secretion of both catecholamines induced by 5 microM nicotine from cultured chromaffin cells. In contrast, over the concentration range 0.1 nM-10 microM, somatostatin had no effect on the secretory responses produced by 10 nM angiotensin II or 1 microM histamine. Inositol phosphate accumulation in cultured bovine adrenal medullary cells was unaffected by 0.1 nM-0.1 microM somatostatin, however at 1 and 10 microM somatostatin it was significantly increased, by 23% and 103% respectively. The effects of somatostatin (0.1 nM-10 microM) and of 50 microM muscarine on inositol phosphate accumulation were simply additive. Similarly, somatostatin at 0.1 nM and 10 nM together with 10 nM angiotensin II or 1 microM histamine produced additive inositol phosphate responses. In contrast, 1 microM somatostatin gave significantly more-than-additive (synergistic) inositol phosphate responses with angiotensin II and histamine. The results suggest that some adrenal medullary cells possess several types of receptors, and that these receptors may interact to produce non-additive responses.

Adrenal Glands↗

The innervation of the adrenal gland. II. The source of spinal afferent nerve fibres to the guinea-pig adrenal gland.

The sensory innervation of the guinea-pig adrenal medulla was studied using the fluorescent retrograde tracer Fast Blue. Labelled neurons were found in the dorsal root ganglia at segments T3-L2, the greatest contribution arising from T10 representing 15.2% of the total number of labelled cells. Labelling was ipsilateral to the site of injection of tracer into the adrenal medulla and the labelled neurons ranged in size between 6 and 36 microns. The overall size distribution fell into two groups of between 6 and 15 microns and of between 18 and 36 microns. Presumed sensory nerve endings were found in the adrenal medulla associated with chromaffin cells and vascular elements. The nerve endings were ovoid to spherical and densely packed with mitochondria. It is concluded that events occurring in the guinea-pig adrenal medulla, and possibly cortex, are monitored by sensory nerve terminals whose cell bodies lie within dorsal root ganglia. The exact distribution of the sensory nerve terminals within the adrenal gland is yet to be determined.

Adrenal Glands↗

Demonstration of glucocorticoid receptors in the adrenal cortex: evidence for a direct dexamethasone suppressive effect on the rat adrenal gland.

The adrenal cortex was evaluated for the presence of glucocorticoid receptors and functions. Substantial binding of [3H]dexamethasone was observed in aminoglutethimide-treated, hypophysectomized, and intact rats. Further studies demonstrated binding in cultured bovine adrenocortical cells and in Y-1 cells, a cloned murine cell line of adrenal cortical origin. Scatchard analysis of specific binding data in cytosol from hypophysectomized rats revealed an apparent Kd of approximately 15 nM and a receptor content (Nmax) of 123 fmol/mg cytosol protein. Analysis of Y-1 cell cytosol showed a Kd of approximately 17 nM and Nmax of 190 fmol/mg protein. The binding site in hypophysectomized rats had the following steroid specificities: high affinity for dexamethasone, corticosterone, and progesterone; moderate affinity for 11 beta-cortisol, and low affinity for testosterone, estradiol, pregnenolone, and 11 alpha-cortisol. Sedimentation in sucrose density gradients revealed 8S binding peaks in cytosols prepared from intact rat adrenal glands, Y-1 cells, and cultured bovine adrenocortical cells. Time- and temperature-dependent nuclear uptake of [3H]dexamethasone in Y-1 cells was demonstrated. In vivo treatment of hypophysectomized rats with dexamethasone significantly enhanced the rate of adrenal atrophy. ACTH stimulation tests in hypophysectomized rats showed a decreased corticosterone response in dexamethasone-treated rats compared to that in control animals. However, in vitro, there was no evidence for an effect of dexamethasone on ACTH-stimulated corticosterone production. The data indicate that the adrenal cortex possesses a high affinity binding site that fulfills the criteria for a glucocorticoid receptor. Glucocorticoid administration enhances adrenal atrophy and impairs adrenal function. We speculate that this action contributes to the suppressive effect of glucocorticoids on the pituitary-adrenal axis.

Adrenal Cortex↗

Anatomy and pathology of the adrenal glands.

The adrenals are paired glands that lie in the retroperitoneum and have a close anatomic relation to the kidneys. Each gland has a cortex and a medulla, which act as separate entities. The adrenals are affected by various pathologic conditions, including congenital abnormalities, hypofunction, nodular enlargement, hyperplasia, and malignant and benign tumors. Newer developments in pathologic evaluation are fine-needle aspiration biopsy, immunohistochemistry, and ploidy and oncogene analysis.

Adrenal Gland Diseases↗

Effect of prolonged physical training on the histochemically demonstrable catecholamines in the sympathetic neurons, the adrenal gland and extra-adrenal catecholamine storing cells of the rat.

The effect of daily physical training for 24 months on the sympathetic neurons, adrenal gland, extra-adrenal catecholamine storing cells and on the heart was investigated in rats. The tissue catecholamine fluorescence intensity was determined by microfluorimetric quantitation of catecholamines. The maximal and final body weights were significantly lower in trained animals. The trained rats showed prominent increase of heart weight relative to body weight, while the adrenals did not enlarge. The adrenergic nerve fiber density of the heart and the fluorescence intensity of the terminal axons were significantly increased. There were no changes in the fluorescence intensity of the perikarya of the sympathetic neurons and the amount of extra-adrenal catecholamine storing cells after physical exercise. The volume of the superior cervical ganglion was doubled and the neuronal perikarya were enlarged in trained animals. The prolonged physical training throughout the life span of the rat gave new information about the reactions of the sympathetic nervous system to physical exercise.

Adrenal Medulla↗