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)

1. Dibutyryl cyclic AMP (Db cAMP, 75-500 microgram/kg), injected into the lateral ventricle of the brain of the cat increased blood pressure, heart rate and splanchnic discharge rate. 2. ATP, but not AMP, induced similar changes; GMP in small doses increased blood pressure. 3. A number of drugs are known to activate adenylate cyclase-induced hypertension, tachycardia and increase splanchnic discharge rate. This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365. 4. Injection into the lateral ventricle of theophylline or Ro 7/2956, both inhibitors of phosphodiesterase, similarly increased blood pressure. 5. Histamine administered by the same route induced similar reactions; it is not known if this action was exerted by activation of H1- or H2-receptors. 6. Somatostatin, known to reduce cAMP levels, induced a small but significant decrease in blood pressure. Melanocyte stimulating hormone release inhibiting factor (MIF) and TSH were ineffective. 7. These results provide evidence for the possibility of a role for cAMP in the central regulation of blood pressure at suprabulbar levels.
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PMID:Cyclic 3'5'-adenosine monophosphate and central circulatory control in cats and dogs. 2 Feb 56

The effect of different environmental temperatures on adenyl cyclase was studied. An increase in temperature appears to increase TRH-induced activity of adenyl cyclase, and possible causes an increases sensitivity to the hormone. Cyclic AMP levels of the pituitaries showed change at different environmental temperatures.
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PMID:Adenyl cyclase activity at different environmental temperatures in the isolated rat anterior pituitary membranes. 18 84

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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PMID:Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances. 19 Feb 56

Synthetic thyrotropin releasing hormone was found to stimulate rat anterior pituitary adenylate cyclase activity. In the presence of guanosine triphosphate, no further stimulation was recorded; guanosine triphosphate alone also increased the adenylate cyclase activity. Prostaglandin E1 was found to stimulate a basal enzyme activity and this effect was significantly enhanced by guanosine triphosphate. It appears that guanosine triphosphate could be a modulator of adenylate cyclase activity in rat anterior pituitary in response to PGE1 but not to TRH.
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PMID:The effect of TRH on the anterior pituitary adenylate-cyclase activity of rat. 82 22

Thyroliberin (TRH), vasoactive intestinal peptide (VIP) and somatostatin (SRIF) act through receptors that are coupled to guanine nucleotide-binding regulatory proteins (G proteins). Regulation of hormone action may occur at the level of G protein coupling to the receptor or effector systems. In this study we demonstrate that prolonged exposure (for up to 48 hr) of cultured rat pituitary adenoma GH3 cells to these hormones caused homologous and to some extent heterologous attenuation of the adenylyl cyclase (AC) (EC 4.6.1.1) responsiveness. In addition, TRH and SRIF diminished both TRH- and guanosine 5'-[beta gamma-imido]-triphosphate-enhanced phospholipase C (PLC) (EC 3.1.4.3) activity within the same time-course. Measurements of cells membrane levels of Gs protein alpha-subunit (Gs alpha), G(i)-1 alpha/G(i)-2 alpha, G(i)-3 alpha, G(o) alpha and G beta by immunoblotting were performed. TRH and VIP upregulated levels of all G proteins except G(o) alpha and G beta. In contrast, SRIF caused a marked reduction of G beta levels. Thus, TRH and VIP, both acting through Gs, both modulated the alpha-subunit levels of this signal transducer, whereas SRIF, which possibly acts through G(i)-2, did not change the steady state level of G(i)-2 alpha. The actions of TRH, VIP and SRIF are multifaceted at the G protein level, where modulations of subtypes not directly involved in their actions may occur. These findings emphasize the complexity expected to be found in the in vivo situation.
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PMID:Hypothalamic hormones modulate G protein levels and second messenger responsiveness in GH3 rat pituitary tumour cells. 135 62

We investigated the effect of interleukin-6 (IL-6) on second messenger systems in anterior pituitary (AP) cells. The acute exposition of membranes derived from the pituitary gland to IL-6 did not modify basal and forskolin-stimulated adenylate cyclase (AC) activity, as well as inositol phosphate (IP) production and free [Ca(++)]i. Preincubation of AP cells with IL-6 for 20 min did not affect basal second messengers levels, while completely abolished the stimulation by VIP of AC activity, partially inhibited forskolin-stimulated cAMP formation and reduced TRH-stimulated IP production. Finally, the pretreatment of AP cells for 20 min with IL-6 also reduced the TRH-induced rise in free [Ca(++)]i.
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PMID:Interleukin 6 modulation of second messenger systems in anterior pituitary cells. 140 45

In GH3 cells and other clonal rat pituitary tumor cells, TRH has been shown to mediate its effects on prolactin release via a rise of cytosolic Ca2+ and activation of protein kinase C. In this study, we examined the role of protein kinase C in TRH-stimulated prolactin release from female rat primary pituitary cell culture. Both TRH and PMA stimulated prolactin release in a dose-dependent manner. When present together at maximal concentrations, TRH and PMA produced an effect which was slightly less than additive. Pretreatment of rat pituitary cells with 10(-6) M PMA for 24 hrs completely down-regulated protein kinase C, since such PMA-pretreated cells did not release prolactin in response to a second dose of PMA. Interestingly, protein kinase C down-regulation had no effect on TRH-induced prolactin release from rat pituitary cells. In contrast, PMA-pretreated GH3 cells did not respond to a subsequent stimulation by either PMA or TRH. Pretreatment of rat pituitary cells with TRH (10(-7) M, 24 hrs) inhibited the subsequent response to TRH, but not PMA. Forskolin, an adenylate cyclase activator, stimulated prolactin release by itself and in a synergistic manner when incubated together with TRH or PMA. The synergistic effects of forskolin on prolactin release was greater in the presence of PMA than TRH. Down-regulation of protein kinase C by PMA pretreatment abolished the synergistic effect produced by PMA and forskolin but had no effect on those generated by TRH and forskolin. sn-1,2-Dioctanylglycerol (DOG) pretreatment attenuated the subsequent response to DOG and PMA but not TRH. The effect of TRH, but not PMA, on prolactin release required the presence of extracellular Ca2+. In conclusion, the mechanism by which TRH causes prolactin release from rat primary pituitary cells is different from that of GH3 cells; the former is a protein kinase C-independent process whereas the latter is at least partially dependent upon the activation of protein kinase C.
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PMID:PMA-sensitive protein kinase C is not necessary in TRH-stimulated prolactin release from female rat primary pituitary cells. 145 79

Interleukin-6 (IL-6) is a pleiotropic cytokine exerting many immunological and non immunological actions. The cytokine binds to a specific receptor, whose activation induces the association with a novel transducer, the glycoprotein gp 130. Here we present our results about the effect of IL-6 on both hormone secretion and second messenger systems at pituitary level, and the production of IL-6 from cells of central nervous system. IL-6 inhibited basal, VIP and TRH-stimulated prolactin (PRL) secretion from single lactotropes, studied by means of reverse hemolytic plaque assay, whereas in primary cultures of anterior pituitary cells, according to the literature, the cytokine stimulated prolactin secretion. IL-6 did not affect basal adenylate cyclase activity, inositol phosphate production, and cytosolic calcium concentration. Conversely, the preincubation of pituitary cells with interleukin-6 for 20 min significantly reduced VIP- and forskolin-stimulated adenylate cyclase activity, as well as inositol phosphate production and free cytosolic calcium increase induced by TRH.
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PMID:Role of interleukin-6 in the neuroendocrine system. 166 73

Adenosine is a potent paracrine/autocrine feedback inhibitor of cell activation in a variety of tissues. Adenosine action was studied in pituitary cells, in which spontaneous electrical activity causes characteristic oscillations of the cytosolic free Ca2+ concentration, [Ca2+]i. Cells of the GH3B6 rat pituitary tumor line were studied by microspectrofluorimetry using the Ca2+ probes indo-1 and fura-2, in part in combination with electrophysiological tight seal whole cell recordings, obtained with the novel approach of patch perforation. It was demonstrated that adenosine receptor activation by N6-(R-phenyl-isopropyl)-adenosine (PIA) caused a block of electrical activity and abolished the ensuing alterations in [Ca2+]i. PIA mimicked the inhibitory action of somatostatin. Adenosine effects are mediated by A1 receptors in these cells and are antagonized by IBMX, an adenosine receptor blocker. PIA also suppressed action potentials that were elicited by the activation of protein kinase C with the phorbol ester PMA, or during the second phase of TRH action. In contrast, no interference was notable on TRH-induced intracellular Ca2+ mobilization. In addition to the abolition of Ca2+ transients, PIA lowers basal [Ca2+]i in some cells. It is proposed that in addition to the inhibition of adenylate cyclase, A1 receptor action on [Ca2+]i is an important element in the control of excitable pituitary cells.
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PMID:Adenosine A1 receptor-induced inhibition of Ca2+ transients linked to action potentials in clonal pituitary cells. 168 Jul 18

To assess the role of cAMP-mediated signal transduction processes in mediation of secretagogue-stimulated GH release, we examined the dose-related effects of the diterpene adenylate cyclase activator forskolin (FSK) in primary monolayer cultures of rat adenohypophyseal cells. In cell cultures prepared from both immature (12 days old) and adult (6 weeks to 4 months old) male or female rats, the dose-related stimulation of GH release by FSK was biphasic. With increasing FSK concentrations from 0.03-3.16 microM, GH release increased progressively to maximal values of 442 +/- 19% and 303 +/- 10% of basal release in cells from immature and adult rats, respectively. FSK concentrations above 3.16 microM induced progressively diminished GH responses, with net inhibition to below basal release evident at 100 microM FSK. FSK stimulated PRL release to a lesser degree than it did GH release; the PRL response to FSK was also biphasic. When maximal stimulatory concentrations (Emax) of FSK and GH-releasing factor (GRF; 10 nM) were added in combination, the GH response was significantly less than the individual response to either secretagogue alone. In response to FSK alone, GRF alone, and FSK plus GRF, GH release was 478 +/- 7%, 583 +/- 11%, and 244 +/- 5%; 278 +/- 4%, 283 +/- 3%, and 175 +/- 2%; and 299 +/- 12%, 351 +/- 5%, and 191 +/- 17% of basal release in cells from 12-day-old, adult male, and adult female rats, respectively (P less than 0.01 for all responses to combined addition vs. the individual responses). Submaximal stimulatory concentrations of GRF added in combination with submaximal FSK elicited partially additive GH responses; the GH response to Emax GRF, on the other hand, was inhibited in a dose-related manner by all concentrations of FSK that by themselves were stimulatory. The GH responses were also suppressed when Emax FSK was added to cultured cells of 12-day-old rats in combination with Emax cholera toxin (2.5 ng/ml) or prostaglandin E2 (10 microM), agents whose actions, like that of GRF, involve adenylate cyclase activation. In contrast, FSK did not suppress but in most cases augmented the maximal GH responses to secretagogues whose action is independent of adenylate cyclase activation: (Bu)2cAMP (0.5 mM), TRH (100 nM), phorbol myristate acetate (50 nM), the Ca2+ ionophore A23187 (250 microM), and the dihydropyridine Ca2+ channel agonist BAY K8644 (10 microM). Indeed, combined addition of FSK with the latter two agents resulted in synergistic stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biphasic action of forskolin on growth hormone and prolactin secretion by rat anterior pituitary cells in vitro. 169 47


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