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:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Addition of somatostatin (SRIF) inhibits corticotropin-releasing factor- and forskolin-stimulated cyclic AMP accumulation and adrenocorticotropin hormone secretion from mouse anterior pituitary tumor cells (AtT-20/D16-16). However, prior exposure of these cells to SRIF reduced the potency of SRIF to inhibit both corticotropin-releasing factor- and forskolin-stimulated cyclic AMP accumulation and adrenocorticotropin hormone release. This SRIF desensitization is time- and concentration-dependent and reversible. Cross-desensitization to SRIF analogs also occurred whereas SRIF pretreatment did not affect the inhibition by SRIF of 8-bromo-cyclic AMP-stimulated adrenocorticotropin hormone release or did it affect basal cyclic AMP levels, protein content or phosphodiesterase activity. These data indicate that SRIF can regulate the sensitivity of its own receptor and that SRIF desensitization may involve either a down-regulation of SRIF receptors or an uncoupling of these inhibitory receptors from adenylate cyclase.
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PMID:Somatostatin desensitization: loss of the ability of somatostatin to inhibit cyclic AMP accumulation and adrenocorticotropin hormone release. 614 43

The effects of forskolin, an adenylate cyclase activator, were investigated on adrenocorticotropin (ACTH) secretion from AtT-20/ D16 -16 mouse pituitary tumor cells. Forskolin increased adenylate cyclase activity in these cells in the absence of added guanyl nucleotide, an effect blocked by somatostatin. Cyclic AMP synthesis and ACTH secretion increased in a concentration-dependent manner, not only in the clonal cells, but in primary cultures of rat anterior pituitary as well. Somatostatin inhibited cyclic AMP synthesis and ACTH secretion in response to forskolin. When forskolin was coapplied with corticotropin releasing factor, cyclic AMP synthesis was potentiated and ACTH secretion additive. The calcium channel blocker, nifedipine, inhibited forskolin, and 8-bromocyclic AMP stimulated ACTH secretion. These data suggest that ACTH secretion may be regulated at the molecular level by changes in cyclic AMP formation, which in turn regulate a calcium gating mechanism.
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PMID:Forskolin stimulates adenylate cyclase activity, cyclic AMP accumulation, and adrenocorticotropin secretion from mouse anterior pituitary tumor cells. 614 27

In rat pars intermedia cells, the rate of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion was so far known to result from a balance between the stimulatory effect of beta-adrenergic agonists and the inhibitory influence of dopaminergic substances. Recently, we have identified a second stimulatory substance, namely corticotropin-releasing factor (CRF). CRF is a potent stimulator of pars intermedia adenylate cyclase activity, cAMP accumulation and alpha-MSH release. A requirement for calcium ions was observed on basal as well as on CRF-induced alpha-MSH secretion. The beta-adrenergic and CRF effects on adenylate cyclase activity, as well as the dopamine inhibition of adenylate cyclase activity, are potentiated by guanine nucleotides (GTP). Stimulation of the beta-adrenergic receptor with isoproterenol causes a rapid loss in cAMP responsiveness, which can be completely blocked by beta-adrenergic antagonists and partially prevented by dopamine. These findings suggest that CRF should now be considered, in addition to beta-adrenergic agents, as a stimulator of the activity of pars intermedia cells and that cAMP is also involved as mediator of its action. Changes of receptor sensitivity, as well as interaction of the two stimulatory receptors with the inhibitory dopaminergic receptor, are involved in the fine control of pars intermedia cell activity. All three receptors appear to exert their action through a common pathway, namely changes of adenylate cyclase activity.
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PMID:Multiple hormonal control of pars intermedia cell activity. 619 67

Ovine corticotropin-releasing factor (CRF) stimulates adenylate cyclase activity in rat anterior pituitary homogenate at an ED50 value of 70 nM. GTP increases the stimulatory effect of CRF on ]32p] cyclic AMP formation in a rat adenohypophysial particulate fraction and in bovine anterior pituitary plasma membranes. The present data show that CRF stimulates adenylate cyclase activity in the anterior pituitary gland at least partly through a guanyl nucleotide-dependent mechanism.
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PMID:Corticotropin-releasing factor stimulants adenylate cyclase activity in the anterior pituitary gland. 629 3

1. A pure population of pars intermedia cells in primary culture was used to study changes in alpha-MSH secretion and cyclic AMP accumulation. 2. Beta-adrenergic agonists and CRF (corticotropin-releasing factor) stimulate alpha-MSH secretion and cyclic AMP accumulation. 3. Dopaminergic agonists inhibit basal as well as (-)isoproterenol- and CRF-induced alpha-MSH secretion and cyclic AMP accumulation. 4. Beta-adrenergic, dopaminergic and CRF receptors regulate pars intermedia cell activity probably through the adenylate cyclase system.
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PMID:beta-Adrenergic, CRF-ergic and dopaminergic mechanisms controlling alpha-MSH secretion in rat pars intermedia cells in primary culture. 629 87

Pretreatment of rat anterior pituitary cells with corticotropin releasing factor (CRF) rapidly and markedly reduced the ability of CRF to restimulate cyclic AMP formation and adrenocorticotropic hormone (ACTH) release. The effect was dependent on the length of time of pretreatment as well as the concentration of CRF. Neither basal nor intracellular immunoreactive ACTH levels nor basal cyclic AMP content were affected. CRF's stimulatory action on cyclic AMP formation and ACTH release recovered within one hour following CRF pretreatment. Forskolin, a compound that directly activates adenylate cyclase also releases ACTH from these cells. Pretreatment with CRF did not alter forskolin-stimulated cyclic AMP accumulation or ACTH secretion. Furthermore, CRF pretreatment did not change epinephrine's ability to increase the release of ACTH. These results indicate that CRF can regulate the responsiveness of its own receptor.
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PMID:Desensitization of corticotropin-releasing factor receptors. 630 92

The role of cyclic AMP in the stimulation of corticotropin (ACTH) release by corticotropin-releasing factor (CRF), angiotensin II (AII), vasopressin (VP), and norepinephrine (NE) was examined in cultured rat anterior pituitary cells. Synthetic CRF rapidly stimulated cyclic AMP production, from 4- to 6-fold in 3 min to a maximum of 10- to 15-fold at 30 min. Stimulation of ACTH release by increasing concentrations of CRF was accompanied by a parallel increase in cyclic AMP formation, with ED50 values of 0.5 and 1.3 nM CRF for ACTH and cyclic AMP, respectively. A good correlation between cyclic AMP formation and ACTH release was also found when pituitary cells were incubated with the synthetic CRF(15-41) fragment, which displayed full agonist activity on both cyclic AMP and ACTH release with about 0.1% of the potency of the intact peptide. In contrast, the CRF(21-41) and CRF(36-41) fragments were completely inactive. The other regulators were less effective stimuli of ACTH release and caused either no change in cyclic AMP (AII and VP) or a 50% decrease in cyclic AMP (NE). Addition of the phosphodiesterase inhibitor, methylisobutylxanthine, increased the sensitivity of the ACTH response to CRF but did not change the responses to AII, VP, and NE. In pituitary membranes, adenylate cyclase activity was stimulated by CRF in a dose-dependent manner with ED50 of 0.28 nM, indicating that the CRF-induced elevation of cyclic AMP production in intact pituitary cells is due to increased cyclic AMP biosynthesis. The intermediate role of cyclic AMP in the stimulation of ACTH release by CRF was further indicated by the dose-related increase in cyclic AMP-dependent protein kinase activity in pituitary cells stimulated by CRF with ED50 of 1.1 nM. These data demonstrate that the action of CRF on ACTH release is mediated by the adenylate cyclase-protein kinase pathway and that the sequence requirement for bioactivity includes the COOH-terminal 27 amino acid residues of the molecule. The other recognized regulators of ACTH release are less effective stimuli than CRF and do not exert their actions on the corticotroph through cyclic AMP-dependent mechanisms.
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PMID:Mechanisms of action of corticotropin-releasing factor and other regulators of corticotropin release in rat pituitary cells. 630 67

Addition of corticotropin-releasing factor (CRF) to membranes from two ACTH-secreting pituitary tumors strikingly increased in a dose-dependent fashion adenylate cyclase (AC) activity. Significant stimulation was already apparent at 10(-9)M CRF. Stimulation of AC activity by CRF in membranes from non-tumoral tissue adjacent to tumoral corticotrophs was considerably lower, and was lacking in membranes from a growth hormone secreting tumor. These data correlated well with in vivo pre-surgery and post-surgery ACTH responsiveness to CRF of the tumor bearing patients. Basal AC activity was higher in pituitary adenomas than in non-tumoral adjacent tissue. It is concluded that 1) a CRF-sensitive AC exists in ACTH-secreting tumor cells and, 2) increased sensitivity to CRF, as evidenced by greater stimulation of AC activity, may be responsible for the increased ACTH output of tumoral corticotrophs.
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PMID:Corticotropin releasing factor stimulates cAMP formation in pituitary corticotropic tumor cells. 631 41

The secretion of ACTH by corticotrophs in the anterior lobe of the rat pituitary gland is under the stimulatory influence of at least three receptors, namely that for peptidic CRF (corticotropin-releasing factor), vasopressin and alpha 1-adrenergic agents. CRF is a potent stimulator of cyclic AMP accumulation as well as adenylate cyclase activity in the rat adenohypophysis, thus suggesting an important role of cyclic AMP as mediator of CRF action on ACTH secretion. Vasopressin causes a 2-fold increase of the stimulatory effect of CRF on ACTH release in rat anterior pituitary cells in culture. The potentiating effects of vasopressin on CRF-induced ACTH release are accompanied by parallel changes of intracellular cyclic AMP levels. Vasopressin, while having no effect on basal cyclic AMP levels, causes a 2-fold increase in CRF-induced cyclic AMP accumulation without affecting the ED50 value of CRF action. ACTH secretion is also stimulated by a typical alpha 1-adrenergic receptor. Epinephrine causes a marked stimulation of ACTH release which is additive to that of CRF. Epinephrine, in analogy with vasopressin, although having no effect alone on basal cyclic AMP levels, causes a marked potentiation of CRF-induced cyclic AMP accumulation. Glucocorticoids cause a near-complete inhibition of epinephrine-induced ACTH secretion within 4 h with the following order of ED50 values: triamcinolone acetonide (0.2 nM) greater than dexamethasone (1.0 nM) much greater than cortisol (11 nM) greater than corticosterone (22 nM). Similar effects are observed for CRF- and vasopressin-induced ACTH release. Although the activity of the pituitary-adrenocortical axis in the rat is highly dependent upon sex steroids, 17 beta-estradiol, 5 alpha-dihydrotestosterone and the pure progestin R5020 have no detectable effect on basal or epinephrine-induced ACTH release, thus illustrating the high degree of specificity of glucocorticoids in their feedback control of ACTH secretion. Moreover, glucocorticoids have no effect on CRF-induced cyclic AMP accumulation, thus indicating that their inhibitory effect is exerted at a step following cyclic AMP accumulation.
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PMID:Interactions between CRF, epinephrine, vasopressin and glucocorticoids in the control of ACTH secretion. 632 61

The ability of vasopressin and related analogs to induce ACTH, beta-endorphin, and beta-lipotropin release was studied in vitro using incubated rat anterior pituitary quarters or a perifused rat isolated anterior pituitary cell column. Vasopressin and its analogs exhibited corticotropin-releasing factor (CRF)-like activity in a rank order which was different from those for vasopressor or antidiuretic activity. Two dissimilar antagonists with antivasopressor activity showed different effects: one possessed CRF-like activity itself, the other blocked the CRF-like activity of vasopressin. Another antagonist with antipressor and also antiantidiuretic activity had no effect when given alone and also didn't block the CRF-like activity of vasopressin. Some analogs were also tested for their effects on cAMP accumulation. Analogs, which possessed CRF-like activity or blocked CRF-like activity of vasopressin, stimulated cAMP accumulation or inhibited vasopressin-stimulated cAMP accumulation in anterior pituitary quarters, respectively. These results imply that the structural requirements of the CRF-like activity of vasopressin differ from those of the pressor and antidiuretic activity. Therefore, it is possible that the pituitary receptors responsible for CRF-like activity of vasopressin represent a separate category of vasopressin receptors which may be linked to an adenylate cyclase.
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PMID:In vitro adrenocorticotropin/beta-endorphin-releasing activity of vasopressin analogs is related neither to pressor nor to antidiuretic activity. 632 32


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