Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While in vitro incubation of dispersed cell preparations of adrenal cell types has been widely used as an experimental model, few studies have addressed the possibility that the enzymic and mechanical treatments involved may affect tissue functions. Using rat adrenal whole capsule tissue, consisting of glomerulosa cells still attached to the connective tissue capsule together with some fasciculata cells, and dispersed glomerulosa cell preparations formed by a variety of enzymic and incubation treatments, striking differences have been demonstrated between the functions of the various preparations in vitro. Under ACTH stimulation, whole capsules produced (ng per pair +/- s.e.) 405 +/- 35 ng aldosterone, 650 +/- 60 ng 18-hydroxycorticosterone (18-OH-B) and 850 +/- 90 ng corticosterone. In cells dispersed by collagenase incubation followed by repeated pipetting and filtration, aldosterone and 18-OH-B yields under ACTH stimulation fell to values less than 10% of those produced by whole tissue, whereas corticosterone values were unchanged. Omitting the filtration step gave a less well marked decline in aldosterone and 18-OH-B to 50% of intact tissue values. When the tissue was not dispersed after collagenase incubation, aldosterone and 18-OH-B outputs were similar in the two preparations. The decline in aldosterone and 18-OH-B is not attributable to loss in cell-cell contact alone, since short term culture of collagenase dispersed cells on contracting collagen discs did not restore the capacity to produce these steroids, and a decline in their output also occurred in similar culture of intact capsule tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Origins of the differences in function of rat adrenal zona glomerulosa cells incubated as intact tissue and as collagenase-prepared cell suspensions. 608 6

The effect of the natrium ionophore, monensin, on aldosterone production was studied using rat adrenal collagenase-dispersed capsular cells. Monensin inhibited aldosterone production in a dose-dependent fashion (10(-9)-10(-6)M). Although monensin inhibited both ACTH- and angiotensin II (AT-II)-stimulated aldosterone production, its inhibitory effect on ACTH-stimulated aldosterone production was greater than that on AT-II-stimulated aldosterone production. The inhibitory effect of monensin on aldosterone production was not accompanied by significant changes in cAMP production. Furthermore, (Bu)2cAMP-stimulated aldosterone production was inhibited by monensin. These results suggest that the inhibitory effect of monensin on aldosterone production is due to an increase in intracellular sodium ion concentration, and that monensin acts at step(s) distal to the generation of cAMP. The differences in the inhibitory effects of monensin on the steroidogenic action of AT-II and that of ACTH may be related to the presence of different steroidogenic mechanisms, including calcium ion dependency.
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PMID:Effect of natrium ionophore on aldosterone production in the rat adrenal gland. 609 48

We investigated the in vitro steroidogenic activity of a new aldosterone-stimulating factor (ASF). Aldosterone responses of adrenal zona glomerulosa cells to ASF were assessed in response to variations in sodium intake and during incubation with either ACTH or angiotensin II (AII). Studies were performed in collagenase-dispersed adrenal capsular cells harvested from male New Zealand White rabbits that were on either regular or low sodium diets for 7-10 days. ASF, AII, and ACTH produced dose-dependent increases in aldosterone production. In cells from sodium-replete rabbits, the concentrations required to elicit the half-maximum response (ED50) were 2.2 +/- 0.3 (+/-SE) X 10(-11), 7.2 +/- 1.1 X 10(-10), and 3.4 +/- 0.5 X 10(-8) M for ACTH, AII, and ASF, respectively. Sodium depletion increased maximal responses but not sensitivity to AII and ACTH; responses to ASF were essentially unchanged. Large concentrations of ASF (10(-7) M) potentiated AII-induced aldosterone responses of adrenal capsular cells from sodium-depleted, but not sodium-replete, rabbits. In marked contrast, similar concentrations of ASF inhibited ACTH-induced aldosterone production of adrenal capsular cells from both sodium-replete and sodium-depleted rabbits. It is concluded that ASF has its own intrinsic steroidogenic activity. Furthermore, although large concentrations of ASF potentiate AII responses in sodium-depleted animals, ASF inhibits the aldosterone-stimulating activity of ACTH in both sodium-replete and sodium-depleted animals.
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PMID:Steroidogenic properties of a new aldosterone-stimulating factor: interaction with angiotensin II and adrenocorticotropin during variations of dietary sodium. 609 49

A 48-year-old man with typical clinical and biochemical features of primary aldosteronism was revealed on operation to have two adrenocortical adenomas in the left gland. An ACTH-dependent pattern of aldosterone secretion was demonstrated in terms of the parallel circadian rhythm of aldosterone with cortisol and the exaggerated response to ACTH but not to angiotensin II. Aldosterone and cyclic AMP release in vitro was studied using collagenase-dispersed cells of each adenoma. Not only the large adenoma but the small one showed basal and ACTH-stimulated releases of aldosterone greater than those by the adjacent tissue. In response to angiotensin II and potassium, the small adenoma showed a larger maximum increment of aldosterone than the large adenoma. This difference in endocrine features of the two adenomas suggests a possible transformation in their nature during development. An exaggerated cyclic AMP release by the adenomas in response to ACTH in vitro suggested the possible role of increased adenylate-cyclase activity in the hyperresponse of aldosterone to ACTH in this case.
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PMID:Endocrine characterization of the adrenal adenomas in a case of primary aldosteronism. 610 Apr 5

Although the biological effects of ketanserin were originally attributed to its specific interaction with serotonin type 2 (5HT2) receptors, at high doses (greater than 10(-8)M) it also appears to act as an alpha 1-antagonist in some tissues. This in vitro study examines the possibility that Ketanserin may inhibit serotonin-induced steroidogenesis by blockade of alpha 1-receptors. Rat zona glomerulosa cells prepared by collagenase digestion of adrenal capsular tissue were incubated at 37 degrees C in Krebs-Ringer bicarbonate buffer (0.2% glucose, 0.2% bovine serum albumin) for 30 min with increasing doses of serotonin (10(-9)-10(-6)M) alone or in the presence of ketanserin (10(-6)M), methysergide (a 5HT-receptor antagonist) 10(-6)M) or prazosin (an alpha 1-antagonist)(10(-6)M). Cyclic AMP, Corticosterone and aldosterone outputs were measured by radioimmunoassay. Serotonin produced correlative sigmoidal dose responses for cyclic AMP, corticosterone and aldosterone which were inhibited by ketanserin and methysergide but not by prazosin. These results suggest that ketanserin does not act by alpha 1-blockade in the adrenal zona glomerulosa but rather as a specific 5HT-receptor antagonist.
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PMID:The specificity of ketanserin in the inhibition of serotonin-induced steroidogenesis in the rat adrenal zona glomerulosa. 610 Jul 54

Primary culture of bovine adrenal subcapsular cells was used to investigate direct effects of catecholamines on aldosterone secretion. Cells dispersed with collagenase and DNAse and cultured at high density (1.5-2 million/ml) for 3 days displayed high sensitivity to angiotensin II and ACTH, with an ED50 of 1.4 and 1.5 nM, respectively. Adrenergic agonists elicited a 4- to 6-fold stimulation of aldosterone secretion with potency order (-)isoproterenol greater than (-)epinephrine equals (-)norepinephrine greater than (+)isoproterenol, and corresponding ED50 5, 240, 213, and 3000 nM, respectively. No reproducible inhibition by dopamine of basal or stimulated levels of aldosterone secretion could be detected, but a weak stimulatory effect was sometimes observed at high concentration greater than 10 microM. (-)Isoproterenol stimulation of aldosterone production was potently inhibited by the beta-adrenergic antagonists (-)alprenolol and (+)alprenolol with potencies of 1.8 and 110 nM, respectively. The alpha-adrenergic antagonists prazosin, yohimbine, and phentolamine only weakly inhibited (-)isoproterenol stimulation with potencies of 5, 13, and 140 microM, respectively. The potent beta 2-adrenergic antagonist ICI 118.551 and the weaker beta 1-adrenergic antagonist atenolol were roughly equipotent with potencies of 0.27 and 0.44 microM, respectively. Addition of the phosphodiesterase inhibitor Ro 20-1724 at 10 microM doubled the maximum stimulation effect of (-)isoproterenol without changing the potency of the catecholamine or the basal level of aldosterone secretion, suggesting a potential role of cAMP as a mediator of isoproterenol stimulation. These results indicate the presence of a beta 1-adrenergic receptor stimulating aldosterone secretion in bovine zona glomerulosa cells. The physiological significance of direct beta-adrenergic stimulation of aldosterone production is currently being assessed.
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PMID:Direct beta-adrenergic stimulation of aldosterone secretion in cultured bovine adrenal subcapsular cells. 614 9

The steroidogenic properties of a glycoprotein fraction (ASF), isolated from normal human urine, were studied in cat adrenal capsular collagenase-dispersed cells and its effects compared to those of ACTH and Angiotensin II (AII). ACTH, AII and ASF induced dose-related increases in both aldosterone and cortisol production. In order of potency, ACTH = AII greater than ASF in stimulating aldosterone production and ACTH greater than AII greater than ASF in stimulating cortisol production. Increases in cAMP accompanied the steroidogenic response to ACTH but not to AII or ASF. The response to AII, but not to ASF, was inhibited (87% of normal) by equimolar concentrations of [Sar1, Thr8]AII, a specific AII antagonist. These results suggest that ASF is a true aldosterone secretagogue and that it initiates steroidogenesis by mechanisms similar to those of AII. However, the inability to block it effect with a specific antagonist of AII provides evidence for its action on a separate receptor site.
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PMID:In vitro steroidogenic properties of a new hypertension-producing compound isolated from normal human urine. 624 62

To elucidate the role of prostaglandins in adrenal steroidogenesis, we studied aldosterone and corticosterone responses to 3 x 10(-8) M--3 x 10(-4) M of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), prostacyclin (PGI2), and arachidonic acid (AA) in collagenase dispersed rat adrenal capsular and decapsular cells. Whereas adrenocorticotrophic hormone (ACTH) and angiotensin II (AII) stimulated aldosterone production in capsular cells and ACTH stimulated corticosterone production in decapsular cells in a dose dependent fashion, aldosterone and corticosterone production were not stimulated significantly by PGE2, PGF2 alpha, PGI2, and AA. Although preincubation of dispersed adrenal cells with indomethacin (3 x 10(-5) M) markedly inhibited PGE2 synthesis, ACTH- and AII-stimulated aldosterone production and ACTH-stimulated corticosterone production were not attenuated despite prostaglandin blockade. These results indicate that prostaglandins are unlikely to play an important role in adrenal steroidogenesis.
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PMID:Effects of prostaglandins on adrenal steroidogenesis in the rat. 624 47

Beta-Lipotropin stimulated the production of aldosterone in collagenase-dispersed rat adrenal capsular cells. The maximum response obtained with beta-lipotropin was the same as the response obtained with corticotropin and was greater than that obtained with angiotensin II. These data suggest that beta-lipotropin may play a role in aldosterone regulation.
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PMID:Beta-lipotropin: a new aldosterone-stimulating factor. 624 63

Angiotensin II (angio II) receptors have been compared using tissues from aldosterone-producing adenomas (APAs), adjacent nontumorus tissue, and normal human adrenal glomerulosa. Plasma membrane-rich subcellular fractions were employed in a radioreceptor assay with [125I]angio II. In vitro aldosterone secretory response to angio II were determined using isolated cells obtained by collagenase digestion. Results are reported as the mean +/- SE. Normal glands have high and low affinity receptor sites for angio II. The Ka values for a normal adrenal obtained at surgery were 2.5 and 0.4 nM-1, while autopsy adrenals were 1.1 +/- 0.4 and 0.3 +/- 0.15 nM-1 (n = 3). APAs and adjacent nontumorous tissue possessed only low affinity receptor sites (0.22 +/- 0.05 nM--1; n = 11). The receptor concentration for a surgically obtained adrenal was 1562 fmol/mg protein, contrasted with 466 +/- 135 from autopsy adrenals. APA and adjacent tissue bound 462 +/- 112 fmol/mg protein. Cells from seven of eight APAs produced aldosterone when stimulated by angio II (3 x 10(-10)-10(-6) m). The increments were 16-105% above basal levels. The response were similar to but less senstive than cells from normal adrenals. The only tumor that failed to respond had 1/50th of the receptors of the other APAs. In contrast, only three of seven adjacent tissues responded, and then only negligibly. ACTH (10(-8) M) increased aldosterone production by APAs 10-158%, by normal cells 283% and by three of six adjacent nontumorous tissues 170-400%. The observations that APAs have angio II receptors and aldosterone responses to angio II is consistent with the fact that some patients with APA have postural increments of plasma posture. The presence of receptors of adjacent tissue and no in vitro response suggest a defect in the aldosterone biosynthetic pathway as a cause of the prolonged absence of response to angio II after removal of APAs.
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PMID:Angiotensin II receptors and in vitro aldosterone responses of aldosterone-producing adenomas, adjacent nontumorous tissue, and normal human adrenal glomerulosa. 625 23


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