Adrenal steroids: new answers, new questions

Science ◽  
1987 ◽  
Vol 237 (4812) ◽  
pp. 236-237 ◽  
Author(s):  
J. Funder
Keyword(s):  
Adrenal Steroids

Ultrastructural Cytopiasmic Changes of Adrenal Cortex During Pregnancy

1969 ◽  
Vol 27 ◽  
pp. 298-299
Author(s):  
T. M. Murad ◽  
Karen Israel ◽  
Jack C. Geer
Keyword(s):  
Adrenal Gland ◽  
Steroid Hormones ◽  
Adrenal Cortex ◽  
Lipid Droplets ◽  
Plasma Cholesterol ◽  
Adrenal Steroids ◽  
Dynamic Changes ◽  
Cortical Cells ◽  
Acetyl Coenzyme A ◽  
Adrenal Cortical Cells

Adrenal steroids are normally synthesized from acetyl coenzyme A via cholesterol. Cholesterol is also shown to enter the adrenal gland and to be localized in the lipid droplets of the adrenal cortical cells. Both pregnenolone and progesterone act as intermediates in the conversion of cholesterol into steroid hormones. During pregnancy an increased level of plasma cholesterol is known to be associated with an increase of the adrenal corticoid and progesterone. The present study is designed to demonstrate whether the adrenal cortical cells show any dynamic changes during pregnancy.

Interaction between cortisol and arachidonic acid on the secretion of LH from ovine pituitary tissue

1991 ◽  
Vol 131 (1) ◽  
pp. 87-94 ◽  
Author(s):  
A. W. Nangalama ◽  
G. P. Moberg
Keyword(s):  
Arachidonic Acid ◽  
Plasma Membrane ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Adrenal Steroids ◽  
Membrane Phospholipids ◽  
Pituitary Tissue ◽  
Receptor Sites ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT In several species, glucocorticoids act directly on the pituitary gonadotroph to suppress the gonadotrophin-releasing hormone (GnRH)-induced secretion of the gonadotrophins, especially LH. A mechanism for this action of these adrenal steroids has not been established, but it appears that the glucocorticoids influence LH release by acting on one or more post-receptor sites. This study investigated whether glucocorticoids disrupt GnRH-induced LH release by altering the liberation of arachidonic acid from plasma membrane phospholipids, a component of GnRH-induced LH release. Using perifused ovine pituitary tissue, it was established that exposure of gonadotrophs to 1–1000 nmol cortisol/l for 4 h or longer significantly reduced GnRH-stimulated LH release with the maximal inhibitory effect being observed after 6 h of exposure to cortisol. This suppressive effect of cortisol could be reversed by administration of arachidonic acid, which in its own right could stimulate LH release from ovine pituitary tissue. Furthermore, the inhibitory effect of cortisol on GnRH-stimulated LH release could be directly correlated with decreased pituitary responsiveness to GnRH-stimulated arachidonic acid liberation, consistent with our hypothesis that glucocorticoids can suppress GnRH-induced secretion of LH by reducing the amount of arachidonic acid available for the exocytotic response of GnRH. Journal of Endocrinology (1991) 131, 87–94

Urinary Excretion of Adrenal Steroids During Excercise in Hot Atmospheres

1958 ◽  
Vol 12 (1) ◽  
pp. 13-16 ◽  
Author(s):  
Kathleen W. Robinson ◽  
W. V. Macfarlane
Keyword(s):  
Urinary Excretion ◽  
Adrenal Steroids

The renin-angiotensin system in kidney development: role of COX-2 and adrenal steroids

2004 ◽  
Vol 181 (4) ◽  
pp. 549-559 ◽  
Author(s):  
B. L. Jensen ◽  
J. Stubbe ◽  
K. Madsen ◽  
F. T. Nielsen ◽  
O. Skott
Keyword(s):  
Kidney Development ◽  
Renin Angiotensin System ◽  
Adrenal Steroids ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Cox 2

A COMPARATIVE STUDY OF ALDOSTERONE AND OTHER ADRENAL STEROIDS IN ADRENALECTOMIZED DOGS1

Endocrinology ◽  
1954 ◽  
Vol 55 (6) ◽  
pp. 813-821 ◽  
Author(s):  
W. W. SWINGLE ◽  
R. MAXWELL ◽  
M. BEN ◽  
C. BAKER ◽  
S. J. LEBRIE ◽  
...  
Keyword(s):  
Comparative Study ◽  
Adrenal Steroids

THE INFLUENCE OF ADRENAL STEROIDS AND CORTICOTROPIN ON MASSIVE MYOCLONIC SEIZURES OF INFANCY

PEDIATRICS ◽  
1963 ◽  
Vol 32 (2) ◽  
pp. 169-174
Author(s):  
Patrick F. Bray
Keyword(s):  
Neurological Deficit ◽  
Prognostic Value ◽  
Rational Expectation ◽  
Initial Response ◽  
Response To Therapy ◽  
Adrenal Steroids ◽  
Focal Neurological Deficit ◽  
Rational Treatment ◽  
Follow Up Study

A 4-year follow-up study is reported on 10 infants whose minor motor seizures were treated intensively with cortisone and/or corticotropin. No correlation was found between the infants' initial clinical and electroencephalographic response to therapy and their follow-up intelligence quotients. The similar initial electroencephalographic findings, contrasted with the marked followup differences in levels of intellectual functioning, illustrate the limited prognostic value of the electroencephalogram in this syndrome. Similarly, no correlation was noted in the patients' initial response to therapy, and the presence or absence of microcephaly or focal neurological deficit. In the absence of any other rational treatment, and despite the dismal prospect suggested by this report and those of others, renewed efforts to treat patients earlier and more intensively with cortisone and corticotropin could be undertaken. However, in the light of 4 years' experience, such an approach might be a reflection more of therapeutic desperation than of rational expectation of good results.

CORTICOSTEROIDS AND ANTIDIURETIC SUBSTANCE IN NEPHROTIC CHILDREN

PEDIATRICS ◽  
1953 ◽  
Vol 12 (3) ◽  
pp. 233-252
Author(s):  
ENRIQUE GALÁN ◽  
MANUEL PÉREZ-STABLE ◽  
ORLANDO GARCÍA FAEZ ◽  
EMILIO UNANUE ◽  
OTTO GARCÍA ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion ◽  
Ascitic Fluid ◽  
Renal Hemodynamics ◽  
Tubular Function ◽  
Urinary Flow ◽  
Adrenal Steroids ◽  
Functional Disturbance ◽  
Urinary Steroids ◽  
Nephrotic Children

The role of tubular reabsorption in the pathogenesis of nephrotic edema led the authors to study the participation of antidiuretic hormone and adrenal steroids in regard to changes in renal hemodynamics and tubular function during different clinical events that may induce an increase or a decrease of urinary flow in nephrotic children. Formaldehydogenic steroids in urine, plasma and ascitic fluid and serum antidiuretic substance were simultaneously studied with clearance tests, electrolyte excretion and plasma constituents through 10 different periods of observations. From previous and present studies on renal function it was found that changes in renal hemodynamics and tubular transport mechanisms are responsible for variations in urinary flow leading to accumulation or disappearance of edema in the nephrotic syndrome. An increase in urinary flow was seen to occur with no change in the GFR but with a marked decrease in the U/P inulin and potassium ratio. Serum antidiuretic substance appeared to correlate closely with antidiuresis. Injection of nephrotic sera into peritoneal cavity of rats was followed by an antidiuretic effect similar to that produced by pitressin and posterior pituitary hormone. Antidiuretic factor seemed to be present in the globulin fraction of plasma proteins. No such effect was seen with intraperitoneal injections of plasma albumin, protein-free filtrate and ascitic fluid. An increase in titer of antidiuretic substance was observed during initial doses of ACTH and the reverse at the onset of diuretic response. Urinary excretion of formaldehydogenic steroids depended partly on diuresis in nephrotic children; this was not so in control cases. The influence of tubular function was suggested by the relationship found between urinary excretion of steroids and the V/Cin and V/Cth ratio and between clearance of steroids and diuresis. The influence of renal functional disturbance prevented a correct evaluation of adrenal activity by estimation of urinary steroids in nephrotic children. During the edematous-oliguric stage of nephrosis and in the absence of any stimulating or depressing effect upon the elaboration of adrenal steroids their urinary excretion was not significantly different from that seen in control cases. Formaldehydogenic steroids did not seem to have a direct role in producing variations of urine flow in nephrotic children. Increase and decrease in diuresis occurred simultaneously with an increase and a decrease in urinary and plasma steroids and vice versa. Formaldehydogenic material was found in variable amounts in the ascitic fluid suggesting an appreciable retention in the increased extracellular fluid during the oliguricedematous stage of the nephrotic syndrome. This material appears to be mostly true adrenal steroids. Potassium excretion was related to urinary steroids in nephrotic children but not in control cases. Potassium clearance was related to glomerular filtration in both control and nephrotic children. At the present time it remains a matter of some speculation of the role that steroids present in extracellular fluids may play in the physiologic and morphologic changes known to occur in the course of the nephrotic syndrome and experimentally reproduced by injection of DOCA to animals.

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