Abstract:The meuse adrenal is more responsive to ACTH than the rat adrenal.The meuse adrenal does not differentiate between concentrations of ACTH in solution, only between total amounts. ACKNOWLEDGEMENTS
“…Previous studies have already shown that calcium is needed for optimal steroid production and release in vitro (Birmingham et at. 1960;Triller & Birmingham, 1965), and it has been suggested from studies on broken cell preparations, which do not respond to ACTH, that the action of calcium is to promote the intramitochondrial synthesis of corticosteroids (see Peron & McCarthy, 1968). However, the present studies on intact glands show that in the absence of extracellular calcium, ACTH is still able to increase steroidogenesis, although steroid output is markedly depressed.…”
Section: Discussionmentioning
confidence: 99%
“…In light of the presumed absence of secretary granules within cortical cells, the findings by Birmingham and her associates (Birmingham, Kurlents, Lane, Muhbstock & Traikov, 1960;Triller & Birmingham, 1965), that calcium is important for optimal steroid production and output from sectioned adrenal glands in response to ACTH and 3'5'-AMP, is of great interest. The present experiments explore the role of calcium in ACTHevoked corticosteroid release from isolated perfused adrenal glands, in order to gain further insight into the nature of the action of calcium in the adrenal cortex and to understand more about the intimate mechanism by which calcium acts in the physiological process of secretion.…”
SUMMARY1. Isolated cat adrenal glands were perfused with Locke solution, and the corticosteroid outputs in response to adrenocorticotrophin (ACTH) were studied.2. Steroid outputs varied with the ACTH concentration, as well as with the duration of exposure to a given ACTH concentration.3. Omission of calcium from the perfusion medium markedly depressed ACTH-evoked steroid release. The steroid output was directly related to the extracellular calcium concentration up to 0 5 mM.4. During a constant exposure to ACTH, steroid output was maintained for at least 2-3 hr, provided that calcium was present in the perfusion medium.5. Strontium, but not barium or magnesium, replaced calcium in maintaining the secretary response to ACTH.6. Magnesium depressed ACTH-evoked secretion in the presence of calcium, and this depression of secretion was antagonized by increasing the calcium concentration.7. Prolonged perfusion with sodium-free or potassium-free solutions did not markedly inhibit steroid output in response to ACTH. Excess potassium (56 mM) did not produce a consistent or marked increase in spontaneous steroid output and did not affect the response to ACTH.8. The steroid content of adrenal glands perfused with Locke solution and exposed to ACTH was about 10 % of the amount which was secreted. By contrast, adrenal glands perfused with calcium-free media and exposed to ACTH contained much higher amounts of steroid, despite the negligible amount secreted.9. These data suggest that calcium plays a critical role in the mechanism of corticosteroid secretion from the adrenal cortex.
“…Previous studies have already shown that calcium is needed for optimal steroid production and release in vitro (Birmingham et at. 1960;Triller & Birmingham, 1965), and it has been suggested from studies on broken cell preparations, which do not respond to ACTH, that the action of calcium is to promote the intramitochondrial synthesis of corticosteroids (see Peron & McCarthy, 1968). However, the present studies on intact glands show that in the absence of extracellular calcium, ACTH is still able to increase steroidogenesis, although steroid output is markedly depressed.…”
Section: Discussionmentioning
confidence: 99%
“…In light of the presumed absence of secretary granules within cortical cells, the findings by Birmingham and her associates (Birmingham, Kurlents, Lane, Muhbstock & Traikov, 1960;Triller & Birmingham, 1965), that calcium is important for optimal steroid production and output from sectioned adrenal glands in response to ACTH and 3'5'-AMP, is of great interest. The present experiments explore the role of calcium in ACTHevoked corticosteroid release from isolated perfused adrenal glands, in order to gain further insight into the nature of the action of calcium in the adrenal cortex and to understand more about the intimate mechanism by which calcium acts in the physiological process of secretion.…”
SUMMARY1. Isolated cat adrenal glands were perfused with Locke solution, and the corticosteroid outputs in response to adrenocorticotrophin (ACTH) were studied.2. Steroid outputs varied with the ACTH concentration, as well as with the duration of exposure to a given ACTH concentration.3. Omission of calcium from the perfusion medium markedly depressed ACTH-evoked steroid release. The steroid output was directly related to the extracellular calcium concentration up to 0 5 mM.4. During a constant exposure to ACTH, steroid output was maintained for at least 2-3 hr, provided that calcium was present in the perfusion medium.5. Strontium, but not barium or magnesium, replaced calcium in maintaining the secretary response to ACTH.6. Magnesium depressed ACTH-evoked secretion in the presence of calcium, and this depression of secretion was antagonized by increasing the calcium concentration.7. Prolonged perfusion with sodium-free or potassium-free solutions did not markedly inhibit steroid output in response to ACTH. Excess potassium (56 mM) did not produce a consistent or marked increase in spontaneous steroid output and did not affect the response to ACTH.8. The steroid content of adrenal glands perfused with Locke solution and exposed to ACTH was about 10 % of the amount which was secreted. By contrast, adrenal glands perfused with calcium-free media and exposed to ACTH contained much higher amounts of steroid, despite the negligible amount secreted.9. These data suggest that calcium plays a critical role in the mechanism of corticosteroid secretion from the adrenal cortex.
A diurnal rhythmicity in plasma corticosterone levels was demonstrated in female BALB/cCrgl and C3H/Crgl mice, with and without mammary tumor virus. Removal of the adrenals followed by metopirone treatment reduced circulating corticoid to non-detectable levels in C3H but not in BALB/c mice. Dexamethasone strains. Neonatal exposure to exogenous hormones failed to cause any obvious change in corticoid levels. Bilateral ovariectomy of these neonatally treated mice at 40 days of age resulted in a subsequent lowering of plasma corticoid levels when compared with intact animals.
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