STUDIES ON THE TIME COURSE OF THE RESPONSE OF THE ADRENAL CORTEX TO HISTAMINE AND COLD

1959 ◽  
Vol 37 (1) ◽  
pp. 399-404
Author(s):  
E. Schönbaum ◽  
W. G. Bruce Casselman ◽  
Rosemary E. Large

Rats were injected with histamine or exposed to cold. In either case there was a transient elevation in the output of corticosteroids by the excised adrenal glands in vitro but a prolonged fall in adrenal ascorbic acid. The return of steroid formation to pre-exposure or even lower rates within three hours was not accompanied by any further change of the concentration of adrenal ascorbic acid.

1959 ◽  
Vol 37 (3) ◽  
pp. 399-404 ◽  
Author(s):  
E. Schönbaum ◽  
W. G. Bruce Casselman ◽  
Rosemary E. Large

Rats were injected with histamine or exposed to cold. In either case there was a transient elevation in the output of corticosteroids by the excised adrenal glands in vitro but a prolonged fall in adrenal ascorbic acid. The return of steroid formation to pre-exposure or even lower rates within three hours was not accompanied by any further change of the concentration of adrenal ascorbic acid.


1952 ◽  
Vol 30 (3) ◽  
pp. 157-162
Author(s):  
A. DesMarais ◽  
J. Leblanc

Histochemical examination of adrenal glands of hypophysectomized rats given both ascorbic acid and ACTH showed an enlargement of the cortex and a decrease of sudanophilic substances, as compared to adrenals of hypophysectomized rats receiving ACTH alone. “In vitro” experiments on incubated slices of adrenal glands have shown that ascorbic acid and ACTH have a synergistic effect on the secretory activity of the cells of the adrenal cortex.


1958 ◽  
Vol 36 (1) ◽  
pp. 571-574
Author(s):  
E. Schönbaum ◽  
W. G. Bruce Casselman

In the adrenal glands of rats given histamine, there are significant correlations between the increase in steroid formation in vitro, and the depletion of ascorbic acid or cytological changes in Z. fasciculata and Z. reticularis indicative of stimulation.


1963 ◽  
Vol 41 (1) ◽  
pp. 597-604 ◽  
Author(s):  
Shail K. Sharma ◽  
R. M. Johnstone ◽  
J. H. Quastel

Uptake of ascorbic acid-1-C14in brain cortex and adrenal cortex slices is an energy-dependent process. Concentration ratios (i.e. ratios of tissue ascorbic acid-1-C14to medium ascorbic acid-1-C14) greater than 4 have been obtained with both tissues in vitro. Ouabain as well as 2, 4-dinitrophenol suppresses ascorbic acid uptake into brain cortex slices.ACTH inhibits the uptake of ascorbic acid-1-C14in adrenal cortex, but not in brain cortex slices. The presence of glucose is necessary for the inhibition. Several cortical steroids, as well as adenosine-3′,5′-monophosphate, at small concentrations inhibit the uptake. The results are consistent with the interpretation that ACTH inhibits the uptake of ascorbic acid in the adrenal cortex through the steroids produced in its presence.


1984 ◽  
Vol 247 (3) ◽  
pp. C234-C239 ◽  
Author(s):  
K. Sato ◽  
F. Sato

The possibility that guanosine 3'5'-cyclic monophosphate (cGMP) may be an intracellular mediator of cholinergic stimulation [methacholine chloride (MCh)] was explored by comparing the relationship between the time course of cGMP accumulation and sweat secretion by use of isolated monkey palm eccrine sweat glands. Isolated sweat glands were incubated with MCh or other agents, and tissue levels of cGMP were determined by radioimmunoassay. In parallel experiments, sweat secretion was induced from cannulated single sweat glands in vitro. Stimulation with MCh produced a Ca-dependent transient elevation of cGMP level from 10 to 80 fmol/gland, peaking at 1-2 min but returning to the basal level by 5 min. The MCh-induced cGMP level was dose dependent and was inhibited by atropine. Ionophore A23187 (2 X 10(-4) M), however, caused persistent elevation of cGMP level for at least 20 min. Neither 10(-4) M MNNG, which elevated the cGMP level comparably with MCh stimulation, nor 8-bromo-cGMP (2 mM) induced sweat secretion. Thus although a parallelism between the cGMP level and sweating rate appears to hold for the initial stage of MCh-induced sweating, it does not hold for the steady state of sweat secretion. Data could not be interpreted to favor the notion that cGMP may be the intracellular mediator of cholinergic sweat secretion.


1983 ◽  
Vol 245 (5) ◽  
pp. E449-E456
Author(s):  
C. Meuli ◽  
J. Muller

Late steps of aldosterone biosynthesis, i.e., the conversions of corticosterone to 18-hydroxycorticosterone and aldosterone, are catalyzed by a mitochondrial cytochrome P-450. Resumption of potassium intake by potassium-depleted rats resulted within 2 days in a marked stimulation of these conversions, as reflected by increased production of aldosterone and 18-hydroxycorticosterone and decreased outputs of deoxycorticosterone, corticosterone, and 18-hydroxy-11-deoxycorticosterone by incubated capsular portions of the adrenal glands. The stimulation of aldosterone biosynthesis was accompanied by the appearance of a protein with a molecular weight of about 49,000 in the mitochondria of the zona glomerulosa but not of the inner zones of the adrenal cortex. Over 48 h of potassium repletion, the amount of this protein increased in parallel with the activity of the final steps of aldosterone biosynthesis. According to its molecular weight, its zone specificity, and the time course of its appearance, this protein might represent the steroid 18-methyl oxidase (cytochrome P-450CMO for corticosterone methyl oxidase) that catalyzes the conversion of corticosterone to 18-hydroxycorticosterone and aldosterone.


1964 ◽  
Vol 92 (3) ◽  
pp. 564-573 ◽  
Author(s):  
SK Sharma ◽  
RM Johnstone ◽  
JH Quastel

1952 ◽  
Vol 8 (3) ◽  
pp. 211-213 ◽  
Author(s):  
S. KAYAHAN

Four grams ascorbic acid given daily by mouth for 4 days increase the urinary excretion of 11-oxysteroids and decrease the excretion of 17-ketosteroids. Ascorbic acid probably acts directly on the adrenal cortex.


1963 ◽  
Vol 41 (3) ◽  
pp. 597-604 ◽  
Author(s):  
Shail K. Sharma ◽  
R. M. Johnstone ◽  
J. H. Quastel

Uptake of ascorbic acid-1-C14in brain cortex and adrenal cortex slices is an energy-dependent process. Concentration ratios (i.e. ratios of tissue ascorbic acid-1-C14to medium ascorbic acid-1-C14) greater than 4 have been obtained with both tissues in vitro. Ouabain as well as 2, 4-dinitrophenol suppresses ascorbic acid uptake into brain cortex slices.ACTH inhibits the uptake of ascorbic acid-1-C14in adrenal cortex, but not in brain cortex slices. The presence of glucose is necessary for the inhibition. Several cortical steroids, as well as adenosine-3′,5′-monophosphate, at small concentrations inhibit the uptake. The results are consistent with the interpretation that ACTH inhibits the uptake of ascorbic acid in the adrenal cortex through the steroids produced in its presence.


1958 ◽  
Vol 36 (6) ◽  
pp. 571-574 ◽  
Author(s):  
E. Schönbaum ◽  
W. G. Bruce Casselman

In the adrenal glands of rats given histamine, there are significant correlations between the increase in steroid formation in vitro, and the depletion of ascorbic acid or cytological changes in Z. fasciculata and Z. reticularis indicative of stimulation.


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