Adrenal Vein Plasma Research Articles

A patient with concurrent primary aldosteronism and Page kidney

The ratio of aldosterone-to-renin activity is currently recommended as a screening test for primary aldosteronism (PA). There are many factors interfering the interpretation of aldosterone-renin ratio (ARR) and could hamper in-time diagnosis of PA. Here, we first report a patient with underlying Page phenomenon and an accidentally disclosed adrenal incidentaloma. High renin secretion from Page phenomenon had masked higher ARR into normal ARR obscuring the diagnosis of PA. However, adrenal venous sampling (AVS) confirmed the autonomous aldosterone secretion with left adrenal vein plasma aldosterone concentration (PAC) 124.1 ng/dl and a lateralization ratio 3.3. AVS may discriminate masked PA due to high renin secretion from Page kidney. It is suggested that clinicians should cautiously interpret aldosterone-renin ratio and consider diagnostic AVS if hyperaldosteronism is highly suspected especially in the background of other secondary hypertension.

Corticosteroids in human blood: IX. Evidence for adrenal secretion of sulfate-conjugated cortisol, 11β,17α-dihydroxy-4-pregnene-3,20-dione-21-yl-sulfate

A method was developed for the estimation of levels of cortisol-21-sulfate (F KS), cortisone-21-sulfate (E KS), and 20(α + β)-reduced cortisol-21-sulfates in blood plasma. Levels of these conjugates were determined in peripheral vein plasma of 42 normal subjects, 21 men, and 21 women (age range 20–64 years) and in adrenal vein plasma of patients with various adrenocortical disorders, six patients with primary hyperaldosteronism, five patients with Cushing's syndrome, and in two obese patients, suspected to have Cushing's syndrome, but with inconclusive laboratory findings. Adrenal vein blood was obtained by percutaneous, trans-femoral adrenal vein catheterization. Levels of non-conjugated (free) cortisol were determined in all plasma samples along with those of the sulfated steroids. F KS was found in all plasma samples, both in men and women. The variation in F KS levels paralleled that in the free cortisol levels, thus the ratio of F K F KS was the same in the blood samples drawn at 8 AM as in those drawn at 4 PM or 5 PM (ranges: 17.5–36.3 in men, 23.6–45.8 in women). The levels of F KS were relatively lower in women than in men (women 610–880 ng/100 mL at AM, 300–510 ng/100 mL at PM; men: 760–1,220 ng/100 mL at AM, 380–760 ng/100 mL at PM). Plasma levels of total sulfate-conjugated Δ 4-3-keto-C-21 steroids (F KS + E KS + 20(α + β)-dihydrocortisol-21-sulfates) were 30–40% higher than those of the levels of cortisol-21-sulfate alone (separated by thin-layer chromatography). In the adrenal vein plasma, levels of Δ 4-3-keto-C-21-steroid-21-yl sulfates were 20 to 40 times higher than levels of these steroids in the peripheral blood. The bulk of the steroid sulfate measured in the adrenal vein plasma consisted of cortisol-21-sulfate. The ratio of F K F KS in the adrenal vein plasma was markedly smaller than in the peripheral vein plasma; it was 6.9–12.3 in males and 4.9–6.7 in females, whereas in the peripheral vein of the same subjects it was 19.2–43.7 in males and 21.4–48.3 in females. Cortisol-21-sulfate isolated from adrenal vein plasma was identified by mass spectrometry. The data presented provide evidence for the secretion of this conjugate by the adrenal cortex. Its secretion appears to be markedly elevated in patients with Cushing's syndrome, both due to hyperplasia and due to adrenal adenoma, as compared with normal subjects and patients with primary aldosteronism, both males and females. However, the F K F KS ratio was markedly lower in Cushing's patients due to adrenal adenoma than due to adrenal hyperplasia, this suggesting that ACTH is stimulating intra-adrenal hydrolysis of cortisol sulfate.

Effects of clonidine, dihydralazine and splanchnic nerve stimulation on the release of neuropeptide Y, MET-enkephalin and catecholamines from dog adrenal medulla

Various neuropeptides are costored together with catecholamines in the adrenal medulla. The concurrent release (evaluated by adrenal vein plasma levels) of these neuropeptides [neuropeptide Y (NPY), met-enkephaline (ME)] and catecholamines [adrenaline (A) and noradrenaline (NA)] from the adrenal gland was examined in chloralose-anesthetized dogs after intravenous administration of clonidine (10 micrograms/kg) and dihydralazine (1 mg/kg). These results were compared to those obtained after the stimulation of the right splanchnic nerve at 1, 5 and 10 Hz frequencies. The increment in the release of catecholamines and neuropeptides was evaluated for dihydralazine and splanchnic nerve stimulation. Dihydralazine (at its maximal effect) induced a significant preferential increase in catecholamines (expressed as mean (SEM): NA: 17.3 (5.4) fold, A: 13.1 (2.6) fold) and ME (16.0 (7.1) fold) versus basal values. However, the significant increase in NPY-LI was only 2.0 (0.4) times the baseline. Splanchnic nerve stimulation induced a frequency-dependent increase in catecholamines and neuropeptides. When the stimulation frequency was increased from 1 Hz to 5 Hz, NA and A levels increased 17.9 (4.3) and 14.0 (2.2) fold, respectively and ME levels 14.1 (3.0) fold. By contrast, NPY-LI was increased only 2.3 (0.3) fold under the same conditions. Increasing the stimulation frequency from 5 Hz to 10 Hz resulted in similar elevations of NA, ME, and NPY-LI adrenal plasma levels (about 4 times) whereas A only increased twice. Clonidine decreased catecholamine and ME adrenal plasma levels (the maximal percent decrease when compared with control values was about 75%) whereas NPY adrenal plasma levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chronic corticotrophin treatment on aldosterone metabolism in the rat.

Chronic treatment with high doses of ACTH leads to marked reduction in aldosterone biosynthesis and secretion both in vivo and in vitro. In contrast, it has been reported that peripheral plasma aldosterone levels may be elevated following prolonged ACTH treatment. The present study attempts to determine the reason(s) for this apparently paradoxical finding. ACTH treatment (40 micrograms/100 g body weight) of male Sprague-Dawley rats for 7 days caused a decrease of more than 90% in aldosterone secretion into the adrenal vein in vivo and aldosterone production by intact adrenal capsules incubated in vitro. In contrast, peripheral plasma aldosterone levels appeared to be increased when measured by radioimmunoassay using two different polyclonal antibodies (antibody 1 (AB1) raised against aldosterone-3-carboxymethyloxime-bovine serum albumin (BSA) and antibody 2 (AB2) raised against aldosterone-21-hemisuccinate-BSA). However, when a highly specific monoclonal antibody (raised against aldosterone-3-carboxymethyloxime-BSA and showing low cross-reactivity to aldosterone metabolites) was used, peripheral plasma aldosterone levels appeared to be reduced in ACTH-treated rats. Following chromatographic fractionation of peripheral plasma, significantly more material with aldosterone-like immuno-reactivity, but which was less polar than authentic aldosterone in chromatographic mobility, was detected in the fractions using antibodies AB1 and AB2. The absence of this material from fractions of adrenal vein plasma leads us to infer that this material is generated in the peripheral circulation, probably as a result of hepatic metabolism. In addition, the overall metabolic clearance rate (MCR) of [3H] aldosterone was found to be significantly decreased following prolonged ACTH treatment. We conclude that the seemingly discrepant findings with regard to the effects of chronic ACTH treatment on peripheral plasma aldosterone levels and the secretion of aldosterone in vivo can be reconciled by (1) the changes in the overall MCR of aldosterone and (2) the generation of increased quantities of aldosterone metabolites such as 5 alpha-dihydroaldosterone and 3 alpha, 5 beta-tetrahydroaldosterone which show significant cross-reactivity with some aldosterone antibodies.

Cryptic Met-enkephalin in adrenal and portal vein during splanchnic artery occlusion shock in cats

Adrenal vein (AD), portal vein (PV), and femoral artery (FA) plasma levels of immunoreactive (IR) Met-enkephalin pentapeptide (ME) and extended ME-IR forms, obtained after sequential incubation of plasma with trypsin and carboxypeptidase B, were examined in 4 cats during splanchnic artery occlusion shock at baseline (S1), during early shock (S2), late shock (S3), and after naloxone (1 mg/kg, i.v.) administration (S4). Early shock (S2) led to a significant increase in levels of extended and fully processed Met-enkephalin IR at all 3 collection sites (AD, PV, FA) without a change in proportional levels of extended Met-enkephalin IR to the pentapeptide IR (ME). Naloxone administration during late shock (S4), however, resulted in a disproportionate increase (150-fold from baseline) in adrenal vein plasma levels of extended Met-enkephalin IR forms, as compared to ME IR (23-fold). In contrast, no changes in plasma levels occurred in PV and FA.

Alpha‐Chloralose Anesthesia Inhibits the Somato‐Sympathetic Reflex Response in Cats More Effectively than Halothan

The effect of halothane anesthesia (H; 0.8 Vol%) or alpha-chloralose anesthesia (AC; 60 mg/kg i.v.) on the somato-sympatho-adrenal reflex response evoked by supramaximal bilateral sciatic nerve stimulation, were examined in two groups of cats (H: n = 6; AC: n = 4). Blood samples were collected simultaneously from the adrenal vein and femoral artery at baseline (S1) and during bilateral sciatic nerve stimulation (S2) for the measurement of norepinephrine, epinephrine, neuropeptide Y, and Metenkephalin, while mean arterial blood pressure (MABP) and heart rate (HR) were recorded. There were no differences between groups at baseline. In halothane anesthetized cats, sciatic nerve stimulation caused significant increases in MABP (S1: 113 +/- 8 mm Hg, S2: 178 +/- 10 mm Hg; mean +/- SE), HR (S1: 223 +/- 15 bpm, S2: 278 +/- 22 bpm), and adrenal vein plasma levels of norepinephrine (S1: 3.1 +/- 0.98 ng/ml, S2: 19.53 +/- 11.5 ng/ml), epinephrine (S1: 15.5 +/- 4.76 ng/ml, S2: 67.31 +/- 14.9 ng/ml), neuropeptide Y (S1: 1.3 +/- 0.12 ng/ml, S2: 2.16 +/- 0.42 ng/ml), and Met-enkephalin (S1: 107 +/- 35.7 pg/ml, S2: 200 +/- 76.5 pg/ml). In contrast, sciatic nerve stimulation in alpha-chloralose anesthetized cats, caused a significant increase only in MABP during sciatic nerve stimulation (S1: 115 +/- 10 mm Hg, S2: 171 +/- 7 mm Hg), while HR and adrenal vein plasma levels of catecholamines, neuropeptide Y and Met-enkephalin remained unchanged from baseline. Adrenal vein epinephrine levels measured during stimulation in the alpha-chloralose group (S2: 6.17 +/- 0.86 ng/ml), were significantly lower as compared to values observed during halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal vein catecholamines and neuropeptides during splanchnic nerve stimulation in cats

Splanchnic nerve stimulation in bursts at low (5 Hz) and high (50 Hz) frequency (30 V, 1 msec; train duration 1 sec; train rate 0.5/second) was employed in 10 cats under halothane anesthesia, during 10-minute periods, while blood samples were concurrently collected from the adrenal vein and femoral artery for the measurement of norepinephrine (NE), epinephrine (EPI), dopamine (DA), Met-enkephalin (ME), neuropeptide Y (NPY), peptide YY (PYY) and neurotensin (NT). In Group I ( n=5 ), splanchnic nerve stimulation was initially applied at 5 Hz followed after 20 min by a 50 Hz stimulus, while in Group II ( n=5 ) the stimulation sequence was reversed. Adrenal vein and femoral artery plasma levels of catecholamines and neuropeptides were not significantly affected by the stimulation sequence, while a significant decrease in blood pressure response was observed in Group II during the 5 Hz stimulation as compared to Group I, indicating desensitization. Splanchnic nerve stimulation at 5 Hz caused a preferential increase in adrenal vein NE (9-fold) versus EPI (7-fold) levels as compared to baseline, while 50 Hz stimulation led to further comparable increases in NE (5-fold) and EPI (6-fold) levels. Significant increases in adrenal vein DA and neuropeptide levels were only observed during 50 Hz stimulation, with DA showing a 5-fold, ME a 2.6-fold and NPY a 3-fold increase as compared to 5 Hz stimulation, and NT a 3.6-fold increase as compared to baseline. Present findings indicate different dynamics in the movement of catecholamines and neuropeptides from the adrenal.

Sympathetic stimulating effects of sufentanil in the cat are mediated centrally

The hemodynamic and adrenal secretory response to sufentanil (25 μg/kg i.v.) was evaluated during halothane anesthesia in 3 groups of cats: group I, n = 5, control; group II, n = 4, naloxone pretreatment (3 mg/kg i.v.); and group III, n = 5, acute spinal transection at T 3–4. Administration of sufentanil in intact cats (group I), caused a significant increase in mean arterial blood pressure and adrenal vein plasma levels of norepinephrine, epinephrine, dopamine, and Met-enkephalin. These effects were abolished in naloxone-pretreated cats (group II). Following spinal transection (group III), sufentanil evoked a significant increase in blood pressure and heart rate, but no change in adrenal hormone levels. Intraventricular injections of sufentanil suggest that these sympathetic stimulating effects are mediated at central sites in proximity to the lateral and third ventricle.

Biochemical characterization of circulating Met-enkephalins in canine endotoxin shock.

The alterations in arterial, venous and adrenal vein levels of immunoreactive Met-enkephalins following endotoxin administration have been investigated in dogs by direct measurement and gel filtration chromatography. Animals were anaesthetized with alpha-chloralose and allowed to breath spontaneously. The left lumbar adrenal vein, limb vein and femoral artery were cannulated for blood sampling. Severe shock was produced by the administration of a large bolus of E. coli endotoxin followed by a continuous infusion. The production of endotoxin shock was associated with significant increases in adrenal vein and systemic venous plasma immunoreactive Met-enkephalin levels. Forty-five minutes after induction of endotoxin shock arterial immunoreactive Met-enkephalin levels were generally higher than baseline values. In resting anaesthetized animals a large 31,000 molecular weight form of Met-enkephalin, presumably proenkephalin, was found in plasma obtained from the adrenal vein, systemic and pulmonary circulations. Following endotoxin this enkephalin-containing peptide still predominated in arterial and venous plasma, whereas in the adrenal vein the proportion of Met-enkephalin immunoreactivity attributable to this large peptide fell. This was associated with the appearance of increasing amounts of smaller molecular forms (18,000, 8000, 3-5000 molecular weight and the pentapeptide itself). In this model enkephalin-containing peptides were not biochemically modified by their passage through the lungs.

Chlorpropamide-ethanol induced met-enkephalin secretion in dogs: release mechanisms and biochemical characterisation

Circulating met-enkephalin-like immunoreactivity (MLI) rises in man after chlorpropamide and ethanol although the origin and molecular forms of circulating MLI are not well defined. We have studied the response to oral ethanol in conscious and anaesthetised dogs pretreated with chlorpropamide. In conscious dogs MLI rose from a basal level of 29 ± 7 pg/ml to a peak of 55 ± 14 pg/ml 10 min after ethanol ( P < 0.001). In anaesthetised animals, following ethanol, plasma MLI rose in caval ( 35 ± 6 pg/ml to a peak of 70 ± 10 pg/ml ), in portal ( 28 ± 6 pg/ml to 51 ± 6 pg/ml ) and in adrenal blood ( 897 ± 316 pg/ml to 1483 ± 298 pg/ml ; P < 0.001). Biogel P-4 chromatography of caval and portal basal plasma showed 87% of MLI measured coeluted with the synthetic pentapeptide, while chromatography of peak plasma showed that only 65% coeluted with the pentapeptide and the remaining 35% was of larger molecular size. Sephadex G75 chromatography of adrenal vein plasma revealed three peaks of MLI of differing molecular sizes ( 8 k = 69.7% ; 3–5 k = 12.1% and the pentapeptide = 18.2%). Treatment of the column fractions with trypsin and carboxypeptidase B resulted in the generation of new MLI with peaks of approximate molecular sizes 31 k (10.4%), and 18 k (37.1%) in addition to 8 k (40.0%), 3–5 k (5.0%) and the pentapeptide (7.5%). Acetaldehyde involvement in MLI release was investigated. Following acetaldehyde infusion, plasma MLI rose both in caval ( 35 ± 9 pg/ml to 86 ± 8 pg/ml ) and adrenal vein ( 417 ± 121 pg/ml to 1768 ± 433 pg/ml ) bloods. Thus we have established an animal model which enables further study of the mechanisms of MLI release and characterisation of the molecular forms. The adrenal medulla, unlike the gut, may be an important source of circulating met-enkephalin and acetaldehyde formation an essential intrinsic component of chlorpropamide-ethanol induced met-enkephalin release.

Primary hyperparathyroidism associated with primary hyperaldosteronism

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.

Pre-operative localization of aldosterone-secreting adrenal adenomas.

Techniques for pro-operative localization of aldosterone-secreting adrenal adenomas were studied in thirty-seven patients, each with hypertension and biochemical evidence of primary hyperaldosteronism and each later having adrenal surgery (thirty-two adenomas, five bilateral hyperplasia). Bilateral adrenal vein catheterization was attempted in all cases; it was successful on the left side in all patients and in 92% of cases on the right. Adrenal vein plasma samples were obtained from the left side in 92% and from the right in 73% of cases. Adrenal vein plasma aldosterone measurements correctly indicated the presence of tumour in twenty-eight cases but falsely predicted unilateral adenoma in two cases of bilateral adrenal hyperplasia. Adrenal venography also correctly predicted unilateral adrenal adenomas in twenty-six cases but falsely suggested the presence of tumour in three cases of bilateral adrenal hyperplasia. Computed tomography (CT) was used in the last eight cases. In seven instances the predictions (six adenomas, one bilateral adrenal hyperplasia) were confirmed at surgery. However, the remaining patient harboured an adenoma 20 mm in diameter which was not detected by CT although diagnosed both by adrenal venography and adrenal vein aldosterone measurements. Ultrasound detected adenoma in only three of twenty-two cases examined. Although further comparative studies of the type described here are required, the results of computed tomography are promising and suggest that this non-invasive technique might well become the first choice procedure in localizing aldosterone-secreting adenomas.

Effect of adrenocorticotropic hormone on extracellular adenosine 3',5'-monophosphate in the hypophysectomized rat.

The effects of ACTH on cyclic AMP levels in peripheral and adrenal vein plasma as well as in adrenal tissue were studied in the hypophysectomized rat and correlated with the steroidogenic response. High doses of ACTH increased adrenal tissue cyclic AMP levels and also markedly elevated cyclic AMP in adrenal vein and peripheral plasma. The gradient between adrenal vein and peripheral plasma cyclic AMP following ACTH was comparable to that observed for corticosterone. Small doses of ACTH produced a maximal rate of steroidogenesis and a several fold elevation in adrenal tissue cyclic AMP, but produced only a slight change in adrenal vein plasma cyclic AMP and no detectable change in peripheral plasma cyclic AMP. The present study indicates that although the adrenal cortex can extrude cyclic AMP in response to ACTH, the gland probably contributes minimally to the extracellular cyclic AMP pool in rats under physiological conditions. (Endocrinology 92: 1502, 1973)

Steroid secretion by the enucleated rat adrenal: measurements during salt retention and the development of hypertension.

It has been shown that rats have an inability to excrete a sodium load following bilateral adrenal enucleation. Rat adrenal vein plasma was analyzed for 18-hydroxy-ll-deoxycorticosterone (18-0H-D0C),1 corticosterone, deoxycorticosterone (DOC), and aldosterone following bilateral adrenal enucleation. All steroids analyzed were secreted in low amounts during the two weeks following enucleation. It appears unlikely that any of these steroids play an important role in the inability to excrete a sodium load which occurs immediately after enucleation. Rat adrenal vein plasma was also analyzed during various stages of adrenal regeneration hypertension. Secretion of all steroids was markedly decreased within 24 hr of enucleation. DOC secretion started to rise at one week and returned to near control levels at three weeks. 18-0H-D0C secretion was markedly diminished during the first three weeks, but greater than control six weeks after enucleation. Corticosterone secretion returned to normal at six weeks, and aldo...

Studies on the dynamics of plasma androgens and on the origin of dihydrotestosterone in dogs.

Testosterone and androstenedione dynamics were studied with a constant infusion technique in adult male dogs. The metabolic clearance rate (1370 ± 660 1/day) and blood production rate (1.5 ± 0.7 mg/day) of testosterone were similar to the metabolic clearance rate (1870 ± 760 1/day) and blood production rate (1.2 ± 0.3 mg/day) of androstenedione. Plasma concentrations of testosterone and androstenedione were respectively 115 ± 46 ng/100 ml and 66 ± 15 ng/100 ml. The conversion of these two prehormones to dihydrotestosterone was studied; respectively, 8.6 ± 2.2 and 1.8 ± 1.1% of plasma testosterone and androstenedione were converted to plasma dihydrotestosterone. In addition, testosterone and dihydrotestosterone were simultaneously measured in peripheral, adrenal and spermatic vein plasma. The concentration of testosterone at these three different sites was 116 ± 18, 98 ± 41 and 6620 ± 2100 ng/100 ml while the concentration of dihydrotestosterone was 34 ± 16, 79 ± 24 and 1710 ± 780 ng/100 ml. From these dat...

Diagnosis and Localization in Primary Aldosteronism

Aldosterone in peripheral and adrenal vein plasma was measured in 21 patients highly suspect for primary aldosteronism. Peripheral and adrenal vein aldosterone levels were measured by a sensitive, accurate radioimmunoassay. Base-line and postfludrocortisone plasma aldosterone values were elevated in all patients while they were supine, with values ranging above normal to very high levels. Adrenal venograms were done in sixteen patients, and a positive radiologic interpretation was made in three fourths. The adrenalvein aldosterone values, however, were diagnostic in all patients. Primary aldosteronism, due to an adenoma, was shown by high levels of aldosterone on the side of the lesion and much lower levels, usually approaching peripheral, on the unaffected side. Aldosteronism due to bilateral hyperplasia appears to be associated with symmetrically elevated levels. These studies suggest that adrenal vein analysis of aldosterone is the most important part of the venogram procedure for localization and diagnosis in primary aldosteronism.

Preferential secretion of adrenaline or noradrenaline by the cat adrenal in vivo in response to different stimuli.

1. The concentrations of adrenaline and noradrenaline in the adrenal vein and the adrenal gland of the cat were studied in response to different stimuli leading to increased catecholamine (CA) secretion.2. Haemorrhage and hypoglycaemia, but not acute exposure to cold or intravenous administration of cocaine, induced considerable increases in total catecholamine secretion.3. The ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma during the control period was higher than the ratio in the adrenal gland itself.4. Haemorrhage increased noradrenaline secretion considerably more than adrenaline secretion so that the ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma was significantly lower than in the adrenal gland itself.5. Hypoglycaemia induced by insulin increased catecholamine secretion, with the adrenaline to noradrenaline ratio significantly higher than in the adrenal gland itself.6. Hypothermia resulted in a fall of the initial high ratio of adrenaline to noradrenaline, to a value similar to that in the adrenal gland.7. Neither cocaine nor changes in adrenal plasma flow affected the adrenaline to noradrenaline ratio in adrenal vein blood.8. It is concluded that preferential release from the adrenal gland of either adrenaline or noradrenaline is possible in vivo in response to different stimuli.

EFFECT OF ANDROGENS AND ANABOLIC STEROIDS ON THE PLASMA DISAPPEARANCE CURVE AND THE DISTRIBUTION OF [1,2-3H CORTICOSTERONE IN THE RAT

ABSTRACT Adult male rats were treated with daily doses (per 100 g of body weight) of 1 mg testosterone propionate (TP), 1 mg 19-nortestosterone phenylpropionate (NTPP), 2 mg methyltestosterone, 2 mg methandrostenolone, or 2 mg stanozolol for 7 consecutive days. Other groups of rats were either castrated or castrated and treated with TP. No differences could be detected between the control and experimental groups with regard to plasma levels of endogenous corticosterone 24 hours after the last doses had been administered. All experimental approaches enhanced the plasma half-life of [1,2-3H] corticosterone. The distribution volume of labelled corticosterone decreased after parenteral TP and NTPP, but increased after oral methandrostenolone and stanozolol. Castration increased the distribution volume but administration of TP to castrated animals normalized this value. Administration of NTPP, methandrostenolone or TP to intact rats for 7 days did not influence the adrenal weight, adrenal corticosterone content, corticosterone level in the adrenal vein plasma, corticosterone secretion rate or the adrenal blood flow.

Human epinephrine secretion. Direct measurement of the secretion of epinephrine from the human adrenal medulla.

ABSTRACT Direct measurements of the secretion of epinephrine from the human adrenal medulla was achieved in conscious patients by the selective catheterization of the left adrenal vein and the analysis of left adrenal vein plasma for norepinephrine and epinephrine. There was an extreme variability in epinephrine secretory rates within the same individual at different points in time as well as variability in epinephrine secretory rates between individuals. It could not be shown that these apparently spontaneous fluctuations in epinephrine secretory rate were due to the injection of angiography dye, changes in the adrenal plasma flow rates, or the experience of pain. They may be due to an intermittent mode of secretion of epinephrine. The data revealed that the human adrenal medulla can selectively release epinephrine without the concomitant release of significant amounts of norepinephrine. The data suggest that normally less than 1% of the epinephrine secreted by the adrenal medulla in a 6-hr period will a...

Studies of androgens and their precursors in adrenocortical virilizing carcinoma.

ABSTRACT A boy with adrenocortical carcinoma has been studied. The initial urinary 17-ketosteroid excretion was between 1700 and 2100 mg/day. Peripheral plasma levels of pregnenolone, 17-hydroxypregnenolone,dehydroepiandrosterone (DHA), androstenediol, testosterone (T) and the sulfate conjugates of these steroids were elevated. Plasma levels of androstenedione (Δ) were also high. The levels of these steroids in adrenal vein plasma were still higher except in the case of unconjugated T. The MCR and the blood production rates of T and Δ were elevated but were lower than their urinary production rates. The urinary production rates of DHAS and DHA were 2000 and 5100 mg/day, respectively. These results, considered in association with the specific activities of several urinary metabolites after injection of tracers (3H-T+14C-Δ, 3H-DHAS+14C-DHA and 3H-DHAS+14C-Δ) suggest that: 1. Urinary androsterone was diluted by precursors that did not pass through the plasma Δ pool. 2. Urinary T glucuronide was derived in pa...