The Biosynthesis of Adrenocortical Steroids

Grant, J. K.

doi:10.1677/joe.0.0410111

Cited by 28 publications

(4 citation statements)

References 70 publications

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“…At submaximal doses of ACTH, glucocorticoid secretion is usually directly correlated with flow through the gland, whether the flow rate is altered by ACTH administration alone (L'Age et al 1970) or by changing pump speed during a perfusion experiment (Porter & Klaiber, 1965;Urquhart, 1965;Sibley et al 1981 We have previously proposed that the capsular and subcapsular arterioles may be the sites at which intraglandular vascular resistance is regulated (Vinson et al 1985/3). The only mechanism which has been proposed to account for the linking of steroidogenesis with blood flow is that the hydrolysis of cholesterol esters consequent on ACTH stimulation releases arachidonic acid which may then be used in the synthesis of prostaglandins (Grant, 1968). However, the consensus of opinion is that prostaglandin production is not increased by ACTH stimulation (Flack, 1973;Swartz, Williams & Butters, 1983), although there are varied reports on the action of indomethacin on ACTH-induced adrenal hyperaemia and steroidogenesis in dogs (Gerber & Nies, 1979;Varga et al 1979).…”

Section: Discussionmentioning

confidence: 99%

Effects of stimulation on steroid output and perfusion medium flow rate in the isolated perfused rat adrenal gland in situ

Hinson¹,

Vinson²,

Whitehouse³

et al. 1986

Journal of Endocrinology

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Using the in-situ, isolated, perfused rat adrenal system, the actions of adrenal stimulants on steroidogenesis and perfusion medium flow rates (under constant perfusion pump conditions) have been studied. In a series of 100 experiments, initial rates of corticosterone output and flow rates were found to be positively correlated, although there was no such relationship between initial rates of aldosterone output and flow rates. Furthermore, in stable perfusion conditions, bolus injections of ACTH increased both flow rate and steroid output in a dose-related manner. In individual experiments there was a clear correlation between corticosterone and flow, but the association between aldosterone secretion rate and flow was less evident. It is possible that this discrepancy arises because of temporal differences in the responses of these two steroids. Flow was also stimulated by dibutyryl cyclic AMP (dbcAMP), with correlations with steroid output similar to ACTH, but the specific zona glomerulosa stimulants angiotensin II amide and potassium ions had, if anything, inhibitory effects on flow, but only at high concentrations. The data suggest that ACTH and dbcAMP evoke specific responses in the adrenal vasculature, resulting in relatively decreased intraglandular vascular resistance. They furthermore suggest that the secretory functions of the inner adrenocortical zones are subject to the additional control of vascular elements in the intact gland.

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Section: Discussionmentioning

confidence: 99%

Effects of stimulation on steroid output and perfusion medium flow rate in the isolated perfused rat adrenal gland in situ

Hinson¹,

Vinson²,

Whitehouse³

et al. 1986

Journal of Endocrinology

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“…1 and 4 are exclusively associated with the mitochondria in adrenal cells, whereas reactions nos. 2 and 3 occur in the cell cytosol and microsomes, respectively (8,9). This sequence is severely limited in the adrenocortical carcinoma 494 (1 5), apparently at a step(s) beyond the formation of CAMP (4).…”

Section: Discussionmentioning

confidence: 99%

“…Corticosteroidogenesis in the normal adrenal gland is a process dependent on several steps. Fractionation studies showed some of these to occur in the mitochondrial fraction and others to occur in the microsomal fraction (8,9). Therefore, it is possible that the reduced rate of steroidogenesis in the tumor may be a result of a defect(s) in one or more of the cell organelles.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructure, Steroidogenic Potential, and Energy Metabolism of the Snell Adrenocortical Carcinoma 494

Kimmel¹,

Péron²,

Haksar³

et al. 1974

The Journal of Cell Biology

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Electron microscope studies were carried out with the adrenocortical carcinoma 494 and normal adrenal cortex tissue. The mitochondria of the tumor cells showed marked differences when compared with mitochondria from fasciculata cells of the normal adrenal cortex. These differences were primarily related to mitochondrial number and crista structure.Corticosterone production in isolated tumor cells was extremely low and neither ACTH nor dibutyryl cyclic AMP had any stimulatory effect. Normal adrenal cells showed at least a tenfold increase under identical conditions. In the presence of corticosteroid precursors the amount of corticosterone produced by the tumor cells was much less than that produced by normal cells.The results indicate a reduced capacity,for l l~-hydroxylation in the tumor mitochondria and a possible reduced capacity for biosynthetic steps before the 1 l~-hydroxylation reaction. Glycolysis in isolated tumor cells was also lower than in normal cells.Isolated tumor mitochondria oxidized succinate normally with a good degree of coupling with phosphorylation. However, unlike normal adrenal mitochondria, the tumor mitochondria showed little or no oxygen uptake with other Krebs cycle substrates. These data suggest that the tumor mitochondria may be lacking in the flavoprotein dehydrogenases responsible for the oxidation of NADH and NADPH, although other components of the respiratory chain may be intact.

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“…In man the main reaction appears to bc 17cr-hydroxylation, followed by 21 and 1 lp-hydroxylation to yield cortisol. In rats, mice and rabbits the 17a-hydroxylating enzyme system seems to be feeble, so corticosterone is the main corticosteroid in these species (GRANT, 1968). Conversion of corticosterone to 11-dehydrocorticosterone in -adrenal gland homogenate of various mammalian species was shown by FAZERAS et al (1970), who localized the highest activity of 11P-hydroxysteroid dehydrogenase in the 105,000 x g sediment.…”

Section: Introductionmentioning

confidence: 95%

Environmental Influences on Corticosterone in Rat Brain. II.In VivoandIn VitroMetabolism

Prisco

Gobbetti

Dessì‐Fulgheri³

et al. 1976

Bolletino di zoologia

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The Biosynthesis of Adrenocortical Steroids

Cited by 28 publications

References 70 publications

Effects of stimulation on steroid output and perfusion medium flow rate in the isolated perfused rat adrenal gland in situ

Effects of stimulation on steroid output and perfusion medium flow rate in the isolated perfused rat adrenal gland in situ

Ultrastructure, Steroidogenic Potential, and Energy Metabolism of the Snell Adrenocortical Carcinoma 494

Environmental Influences on Corticosterone in Rat Brain. II.In VivoandIn VitroMetabolism

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