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)

In human blood platelets, thromboxane A2, prostaglandin E2, and its analogue enprostil activate protein kinase C and promote the second phase of aggregation, whereas prostacyclin and prostaglandin E1 activate adenylate cyclase and inhibit aggregation. In each case, a characteristic group of proteins is phosphorylated following agonist binding. These observations may be related to the inhibitory effect of enprostil on the activation of adenylate cyclase in gastric parietal cells, which follows binding of histamine to H2 receptors. Another system in which enprostil opposes the effect of histamine is the microvasculature. Histamine binds to H1 sites on endothelial cells and induces changes in their shape that allow macromolecules to pass between them into the extravascular compartment. This effect may be mediated by activation of protein kinase C. Pretreatment with enprostil antagonizes the increase in vascular permeability induced by histamine and presumably other inflammatory mediators. Preservation of the integrity of the microvasculature of the gastric mucosa against the effects of cyclo-oxygenase inhibitors, ethanol, and other damaging agents may contribute to the mucosal protective effects of enprostil and some other prostaglandins.
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PMID:Effects of enprostil on platelets, endothelial cells, and other cell types, and second messenger systems by which these effects are mediated. 309 52

The effects of a reserpine treatment inducing supersensitivity to the cardiac effects of agonists (2.5 mg/kg per day for 2 days) was studied on guinea-pig cardiac adenylate cyclase (AC) activity. Reserpine treatment had no effect on basal or Gpp(NH)p (10(-7) M)-stimulated activities. Histamine (2 X 10(-6) and 10(-4) M) stimulation of guinea-pig AC was not influenced by the reserpine treatment. Epinephrine stimulation of AC was affected by reserpine and was characterized by an upward shift of the epinephrine dose-response curve with no change in the epinephrine EC50. The results indicate that the enhancement of cyclic AMP production is an important factor in the reserpine-induced cardiac supersensitivity to beta-adrenoceptor agonists.
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PMID:Reserpine-induced supersensitivity in adenylate cyclase preparations from guinea-pig heart. 365 43

Since in vivo pancreatic glucagon inhibits gastric acid secretion it was of interest to test its direct effect on human parietal cell function in vitro by measuring adenylate cyclase (AC) activity and H+ production. Cells were isolated from human gastric mucosa obtained at surgery for peptic ulcer. In enriched (75%) parietal cells glucagon and histamine stimulated AC much more effectively than in the parietal cell depleted (15%, 7%) fractions. In contrast basal and histamine-stimulated [14C] aminopyrine uptake, an indirect measure of parietal cell H+ production, was not affected by glucagon. In homogenates of mucosal biopsy specimens 2 X 10(-7) mol/l glucagon enhanced AC activity by 76% (corpus) and 20% (antrum), respectively; in the same homogenates 10(-4) mol/l histamine caused a stimulation by 161% (corpus) and 38% (antrum). In fundic biopsy specimens glucagon displayed a biphasic concentration response curve with an increase at 10(-10) mol/l (46% above basal AC activity) and a maximum at 2 X 10(-7) mol/l (97%); histamine elicited the maximal response (192%) at 10(-3) mol/l. Histamine (10(-5), 10(-4), 10(-3) mol/l) and glucagon (10(-10) to 10(-6) mol/l) caused additive stimulation of AC. Ranitidine did not change AC in response to glucagon but abolished the effect of histamine. Our data demonstrate that glucagon stimulates an AC bound to the parietal cells. This response is not blocked by ranitidine suggesting that the glucagon action is mediated by a separate receptor, possibly by a glucagon-receptor. Furthermore we have shown that glucagon in contrast to its effects on AC does not affect H+ production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glucagon and histamine on human parietal cells. 372 3

Histamine stimulated adenylate cyclase from guinea-pig fundic mucosa and 3H-tiotidine binding in guinea-pig cerebral cortex were used to assess the in-vitro histamine H2-activity of the novel H2-antagonist HUK 978. The results showed that HUK 978 was a more potent H2-antagonist than either cimetidine or ranitidine. HUK 978 was also shown to be devoid of activity at the histamine H1-receptor, the muscarinic receptor and the alpha and beta-adrenergic receptors.
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PMID:In vitro histamine H2-antagonist activity of the novel compound HUK 978. 384 May 59

Role of histaminergic mechanisms in the regulation of blood-brain barrier (BBB) was assessed in dog. Histamine increased the entry of sodium fluorescein from the blood to the cerebrospinal fluid (CSF) in a dose-dependent manner. Histamine receptor antagonists, mepyramine (H1) and metiamide (H2) per se did not affect the entry of dye in the CSF. Mepyramine failed to affect the change induced by histamine whereas metiamide completely blocked the histamine-induced entry of sodium fluorescein in CSF. 2-Methyl histamine, a specific H1-agonist, did not affect the barrier permeability. However, 4-methyl histamine, a specific H2 receptor agonist significantly increased the permeability of BBB. This increase was blocked by metiamide. Forskolin, a stimulant of adenylate cyclase, also increased the entry of dye in the CSF which could be significantly blocked by metiamide. It is concluded that histamine increases the permeability of BBB by affecting H2-receptors linked to adenylate cyclase.
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PMID:Evidence for the involvement of histamine in the regulation of blood-brain barrier permeability. 404 Feb 47

In a cell-free system prepared from guinea pig gastric mucosa, histamine and Nalpha-methyl-histamine produced dose-dependent stimulation of cyclic AMP formation and 1,4-methylhistamine had a minimal stimulatory effect. N-methyl-N'-(2-[5-methylimidazole-4-yl-methylthio]-ethyl) -thiourea (metiamide), a new H2 receptor inhibitor, selectively blocked the stimulation of adenylate cyclase by histamine and its active methyl derivative but had no substantial effect on the basal adenylate cyclase activity or adenylate cyclase stimulated by sodium fluoride. Metiamide inhibited the histamine stimulation of adenylate cyclase at 1/100 the concentration of the histamine. Histamine, its methyl derivatives, and metiamide did not influence the activity of cyclic AMP phosphodiesterase from gastric mucosa. Therefore, histamine stimulates gastric mucosal adenylate cyclase via interaction with the H2 receptor without influencing cyclic AMP breakdown, and N-methylation of histamine on the side chain preserves or even increases its stimulating ability. On the other hand, N-methylation in the ring nearly abolishes the ability of histamine to interact with the H2 receptor.
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PMID:Effect of histamine and its methyl derivatives on cyclic AMP metabolism in gastric mucosa and its blockade by an H2 receptor antagonist. 414 25

Histamine has positive inotropic and chronotropic effects on the heart which are not abolished by beta adrenergic-blocking agents. Since the positive inotropic and chronotropic effects of other hormones on the heart are thought to be mediated by cyclic 3',5'-AMP, we examined the effect of histamine on adenyl cyclase in particulate preparations of guinea pig, cat, and human myocardium. Histamine at the peak of its dose-response curve, 3 x 10(-4)moles/liter, produced approximately a 300% increase in cyclic 3',5'-AMP accumulation in the guinea pig, 60% in the cat, and 90% in the human heart particles. Half-maximal activity for the histamine mediated activation of adenyl cyclase in the guinea pig was 9 x 10(-6)moles/liter, almost identical with that observed for norepinephrine in the same preparation. DL-Propranolol, 1 x 10(-5)moles/liter, did not abolish the activation of adenyl cyclase produced by histamine but did abolish the activation produced by norepinephrine. In contrast, diphenhydramine hydrochloride, Benadryl, 8 x 10(-5)moles/liter, abolished the activation of adenyl cyclase by histamine but not that produced by norepinephrine. These data suggest that there are at least two receptor sites in guinea pig heart mediating the activation of adenyl cyclase, one responsive to histamine, the other to norepinephrine. In addition, combined maximal doses of histamine and norepinephrine produced completely additive effects on the activation of adenyl cyclase, which suggests that at least two separate adenyl cyclase systems are present in the heart, each responsive to one of these hormones. However, definitive proof would require physical separation of the two enzymes.
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PMID:Activation of myocardial adenyl cyclase by histamine in guinea pig, cat, and human heart. 432 70

Histamine, beta-adrenergic amines, and prostaglandins inhibited hemolytic plaque formation by splenic leukocytes from immunized mice. The same agents had previously been shown to prevent both the IgE-mediated release of histamine from human basophils and the immunologically specific cytolytic activity of murine lymphocytes, through stimulation of the production of cyclic AMP in leukocytes. We therefore tested the hypothesis that cyclic AMP might mediate an inhibitory effect of these drugs by comparing the ability of these agents to inhibit plaque formation with their effects on cyclic AMP accumulation in leukocytes. In splenic cells from three mouse strains, the dose-dependent effects of these agents of cyclic AMP correlated with their inhibition of plaque formation. Beta- but not alpha-adrenergic agonists were effective in both systems, and the effects of isoproterenol were inhibited by propranolol. Histamine was approximately equipotent with isoproterenol in both systems. Two prostaglandins (E(1) and E(2)) were effective in both systems, but prostaglandin F(2alpha) was not. Dibutyryl cyclic AMP, a lipid-soluble analog of the endogenous nucleotide, inhibited plaque formation by cells of all three strains. Theophylline, an inhibitor of cyclic AMP degradation, inhibited plaque formation slightly, but potentiated the effects of histamine, isoproterenol, and the prostaglandins on both cyclic AMP accumulation and plaque formation. Finally, cholera enterotoxin, a potent activator of adenyl cyclase, produced a delayed inhibition of plaque formation and a parallel increase in leukocyte cyclic AMP content; both effects of the toxin were blocked by canine antitoxin. These results suggest that leukocyte cyclic AMP may act as a "second messenger" to suppress plaque formation in vitro. The inhibitory effects of hormones and cyclic AMP on plaque formation are strikingly similar to their effects on in vitro models of immediate and cell-mediated hypersensitivity. The physiologic significance of these findings is not yet known.
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PMID:Hemolytic plaque formation by leukocytes in vitro. Control by vasoactive hormones. 435 9

Histamine, 4-methylhistamine, 3-(beta-aminoethyl)-1,2,4 triazole and betazole, in that order, stimulated adenylate cyclase prepared from rat gastric tissue in a dose-dependent manner. Burimamide, an H(2)-receptor blocking agent, in concentrations of 1-5 x 10(-6) M antagonized this effect. The data lend some support to the hypothesis that elevated levels of cyclic adenosine 3',5'-monophosphate may be involved in histamine-stimulated gastric secretions and that H(2)-receptors are associated with adenylate cyclase.
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PMID:Stimulation of rat gastric adenylate cyclase by histamine and histamine analogues and blockade by burimamide. 445 68

Short-term treatment of cultured HGT-1 cells with histamine produced a time-dependent (half-life: 20 min) and homologous desensitization of histamine H2 receptor activity mediating cAMP generation in HGT-1 cells and gastric acid secretion in normal gastric mucosa. Histamine treatment resulted in loss of response of the adenylate cyclase to histamine in purified plasma membranes, but had no effect on basal, vasoactive intestinal peptide (VIP)- or NaF-stimulated enzyme activities. We propose that the desensitization of gastric histamine H2 receptor by histamine evidenced in cellular or subcellular preparations from HGT-1 cells could be involved in the physiological regulation and pharmacological control of gastric cell function in man.
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PMID:Desensitization by histamine of H2 receptor-mediated adenylate cyclase activation in the human gastric cancer cell line HGT-1. 609 45


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