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)

The existence of a histamine H2-receptor in the thyroid was investigated. Histamine in vitro stimulated the formation of cyclic AMP and colloid droplet formation in mouse thyroid lobes. Stimulation by histamine of cyclic AMP formation in mouse thyroid lobes was significantly inhibited by metiamide, a histamine H2-receptor antagonist. 4-Methylhistamine, a histamine H2-receptor agonist, markedly stimulated cyclic AMP formation, whereas 2-methylhistamine, a histamine H1-receptor agonist, was ineffective. The stimulation by 4-methylhistamine of cyclic AMP formation was markedly inhibited by metiamide, but not by chlorpheniramine, a histamine H1-receptor antagonist. In contrast, metiamide did not affect cyclic AMP formation induced either by TSH or by the long-acting thyroid stimulator. Therefore, it is suggested that there exists a histamine H2-receptor in the membranes of the thyroid follicular cells which facilitate thyroid hormone secretion via the adenylate cyclase-cyclic AMP system.
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PMID:Evidence for the existence of a histamine H2-receptor in the mouse thyroid. 18 8

A method is described for the preparation of parietal cell-enriched suspensions from dog gastric mucosa. Histamine and E type prostaglandins produce an elevation of cyclic AMP concentration in mixed cell preparations. Parietal cell-rich fractions respond to histamine but only weakly to prostaglandins whilst in fractions virtually free from parietal cells the converse is observed. Prostaglandins which are good antisecretory agents, PGE1, PGE2 and 16,16 dimethyl PGE2 are potent inhibitors of the histamine elevations of cyclic AMP in parietal cell-rich fractions, whilst PFG2alpha shows 1% of their potency. The experiments described support the view that histamine stimulates gastric acid secretion by excitation of an H2-receptor adenylate cyclase system in the plasma membrane of the parietal cell and that acid secretory inhibition by prostaglandins is a result of inhibition of that system.
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PMID:The localization of a histamine H2-receptor adenylate cyclase system in canine parietal cells and its inhibition by prostaglandins. 21 Jun 40

The existence of aminergic receptors in mouse Ehrlich ascites tumor cells was studied. L-Isoproterenol in vitro stimulated the formation of cAMP in isolated Ehrlich ascites tumor cells. Stimulation by isoproterenol of cAMP formation was not significantly inhibited by practolol, a beta1-adrenoceptor antagonist-Salbutamol, a beta2-adrenoceptor agonist, markedly stimulated the formation of cAMP in Ehrlich ascites tumor cells at concentrations from 10(-8)-10(-3) M. After the addition of salbutamol, cAMP levels reached a maximum in 10 min and declined to about 2-fold of the basal level to 30 min. The stimulation by salbutamol of cAMP formation was markedly inhibited by butoxamine, a beta2-adrenoceptor antagonist, but not by practolol. Furthermore, the effect of a maximal dose of salbutamol was additive to that of prostaglandin E2. Histamine and 4-methylhistamine, a histamine H2 receptor agonist, had no significant effects. Therefore, it is suggested that a beta2-adrenergic receptor exists in the membranes of Ehrlich ascites tumor cells in terms of the adenylate cyclase-cAMP system.
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PMID:Evidence for activation by beta2-adrenergic receptors of adenosine 3',5'-monophosphate formation in Ehrlich ascites tumor cells. 21 68

Histamine and epinephrine stimulate the activity of guinea pig heart adenylate cyclase [ATP pyrophosphate-lyase (cyclizing) EC 4.6.1.1], in part, by decreasing the requirement for Mg2+ as an activator. This effect may represent an increase in affinity for Mg2+ and/or a decrease in sensitivity of the enzyme towards inhibition by free ATP. Both of these inotropic hormones also increase maximum velocity. Pretreatment of the membrane-bound enzyme with EDTA, to remove available divalent cations, almost eliminates persistent stimulation by guanyl-5'-yl imidodiphosphate [Gpp(NH)p]. Addition of Mg2+ to the preincubation medium restores the capacity of Gpp(NH)p to acutely activate the enzyme. These results indicate that Mg2+ interacts with the nucleotide (GTP) regulatory site. Persistent stimulation of the enzyme by either Gpp(NH)p or fluoride ion also involves a decrease in the requirement for Mg2+ and an increase in maximum velocity.
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PMID:Activation of cardiac adenylate cyclase: horminal modification of the magnesium ion requirement. 26 97

The effects of histamine, Nalpha-dimethylhistamine, 4,5-methylhistamine, Ntau-methylhistamine, pentagastrin, carbachol, and NaF on the adenylate cyclase activity from canine gastric mucosa were investigated in cell-free preparations. In gastric fundic mucosa, histamine (10(-4) M), Nalpha-dimethylhistamine (10(-4) M), 4,5-methylhistamine (10(-4 M), and NaF (10)-2) M) significantly (P less than 0.001) increased adenylate cyclase activity (means+/-SE) by 44.7+/-6.6, 49.4+/-6.7, 34.0+/-6.4, and 572.0+/-100%, respectively, above basal activity. The effect of histamine and Na-dimethyl histamine was dose-dependent. In contrast, other tested agents failed to stimulate the formation of cyclic AMP in gastric fundic mucosa. Metiamide (10(-4) M) blocked the stimulation of fundic mucosa adenylate cyclase by histamine and Nalpha-dimethylhistamine, without significantly altering basal and NaF-induced adenylate cyclase activity. Histamine, however, did not stimulate the adenylate cyclase activity from the gastric antral mucosa. The findings support the proposal that the canine gastric acid response to histamine may be mediated by cyclic AMP formed in response to stimulation of histamine H2-receptors.
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PMID:Effect of histamine on canine gastric mucosal adenylate cyclase. 83 1

The activity of the non-stimulated, basal adenylate cyclase of the dog gastric mucosa is reduced by the histamine H2-receptor antagonist metiamide but not by the histamine H1-receptor antagonist mepyramine. Histamine activates the adenylate cyclase only slightly. In the presence of 10(-5) M metiamide a concentration-dependent stimulation of the enzyme by histamine was found. These data indicate that endogenous histamine in dog gastric mucosal homogenate is contributing at least in part to what is measured as "basal" adenylate cyclase activity. This effect is mediated by H2-receptor excitation and in earlier studies has prevented the demonstration of a stimulatory effect of exogenous histamine on this enzyme.
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PMID:Adenylate cyclase of the dog gastric mucosa: stimulation by histamine and inhibition by metiamide. 101 40

The effect of epinephrine and histamine on adenylate cyclase activity in lungs and hearts of control and ovalbumin-sensitized guinea pigs was investigated. Epinephrine at 10(-6) M concentration stimulated adenylate cyclase from both organs of the sensitized animals but had no effect on the enzyme from control tissues. At 10(-4) M, epinephrine stimulated equally the enzyme activity from the control and sensitized lungs and hearts. Histamine, 10(-6) and 10(-4), stimulated equally adenylate cyclase in tissues from both groups of animals. The results suggest that ovalbumin sensitization leads to hypersensitivity of the beta-adrenergic receptors to epinephrine without changing their sensitivity to histamine.
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PMID:Adenylate cyclase activity in heart and lung: effect of epinephrine and histamine in control and sensitized guinea pigs. 101 92

Histamine and three histamine analogs (4-methylhistamine, 3-beta-aminoethyl 1,2,4 triazole (TD) and betazole) all produced relaxation in depolarized rat uterine strips. The rank order obtained was the same as that noted previously in the heart and gastric mucosa and the effects of the agonists were blocked by burimamide. The uterine histamine receptor thus appears to be of the H2-type. Adenylate cyclase prepared from the uterus was not stimulated by histamine. Uterine H2-receptors thus do not appear to be associated with adenylate cyclase.
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PMID:Histamine2 receptors in rat uterus. 117 32

Histamine acts on airway contractile elements through at least two different receptor subtypes: H1, which mediates Ca(2+)-dependent contraction, and H2, which stimulates cyclic adenosine monophosphate (cAMP) synthesis and possibly relaxation. The aim of this study was to determine the relative contribution of the different receptor subtypes to histamine-stimulated cAMP production by guinea pig tracheal smooth muscle (GPTSM) cells in primary culture. Histamine and N-alpha-methylhistamine induced concentration-dependent cAMP synthesis; these effects were entirely blocked by 10(-4) M cimetidine, an H2-receptor antagonist, whereas 10(-6) M thioperamide, a selective H3 blocker, was ineffective. The H3 agonist, R-(alpha)-methylhistamine, did not stimulate cAMP synthesis. Triprolidine, an H1 antagonist, did not modify histamine (10(-5) M)-stimulated cAMP synthesis. Histamine (10(-5) M) doubled [Ca2+]i in GPTSM. A 24-h pretreatment of GPTSM cells with 10(-6) M dexamethasone enhanced cAMP synthesized in response to 10(-5) M histamine and to 5 x 10(-6) M forskolin but did not significantly alter either the affinity or the binding capacity for [3H]-tiotidine, an H2-receptor antagonist. These results indicate that GPTSM cells in culture express H2 but not H3 receptors, which are linked to adenylate cyclase; their functional expression does not seem to be modulated by the concurrent activation of H1 receptors, whose presence in GPTSM is evidenced by a histamine-stimulated increase in [Ca2+]i. The most likely site of action of dexamethasone in enhancing histamine-stimulated cAMP synthesis is at the level of adenylate cyclase since the steroid had no effect on the H2 receptor itself.
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PMID:Identification of adenylate cyclase-coupled histamine H2 receptors in guinea pig tracheal smooth muscle cells in culture and the effect of dexamethasone. 133 44

Histamine H1- and H2-receptors have been classically associated with two distinct intracellular second messenger systems. H2-receptors are coupled via a Gs regulatory protein to adenylate cyclase and stimulate cyclic AMP formation, while H1-receptors mediate many of their effects via the products of inositol phospholipid hydrolysis. It is becoming clear, however, that there is a substantial 'cross-talk' between these intracellular second messenger systems in a number of tissues. In guinea-pig cerebral cortical slices, H1-receptor stimulation can augment the direct cyclic AMP responses to adenosine or H2-receptor stimulation via a mechanism which appears to involve both products of inositol phospholipid hydrolysis, inositol triphosphate and diacylglycerol. In contrast, a reverse interaction can occur in bovine tracheal smooth muscle and agents which raise intracellular cyclic AMP levels can inhibit H1-receptor-mediated inositol phospholipid hydrolysis. In addition to these interactions between cyclic AMP and phosphoinositide signalling systems, the H1-receptor-mediated inositol phospholipid response in mammalian cerebral cortex can be regulated (both positively and negatively) via mechanisms which do not involve changes in cyclic AMP levels.
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PMID:Histamine receptors and interactions between second messenger transduction systems. 164 27


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