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)

Pertussis toxin, a substance known to inactivate the inhibitory guanine nucleotide regulatory unit of adenylate cyclase, was injected into the lateral cerebral ventricle of rats; intracellular recordings were made from locus coeruleus neurons in brain slices 1-3 days later. Morphine (an opiate agonist) and clonidine (an alpha 2-agonist) produced the expected outward currents (and associated hyperpolarization and inhibition of firing) in controls whereas the effects of both agonists were blocked in animals pretreated with pertussis toxin. These results are consistent with the hypothesis that opiate and alpha 2-agonists may depress the firing of locus coeruleus neurons by inhibiting adenylate cyclase via a guanine nucleotide regulatory protein.
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PMID:Pertussis toxin blocks the outward currents evoked by opiate and alpha 2-agonists in locus coeruleus neurons. 369 68

Cells of the 7315c tumor released immunoreactive PRL (IR-PRL). Cholera toxin enhanced this release. Morphine and other opiate agonists inhibited IR-PRL release from both untreated and cholera toxin-treated tumor cells. The opiate-induced inhibition of IR-PRL release was concentration dependent and naloxone sensitive. Cholera toxin also enhanced the adenylate cyclase activity of 7315c tumor tissue. Opiates inhibited enzyme activity in both untreated and cholera toxin-treated 7315c tissue in a concentration-dependent and naloxone-sensitive manner. FK 33824 was more potent than [D-Ala2,D-Leu5]enkephalin in inhibiting IR-PRL release and adenylate cyclase activity. In cholera toxin-treated 7315c tumor tissue, GTP was required for opiate-induced inhibition of adenylate cyclase activity. Nonhydrolyzable analogs of GTP inhibited toxin-stimulated cyclase activity in the absence of an opiate. These results suggest that the 7315c tumor possesses a mu-opiate receptor; stimulation of this receptor inhibits both IR-PRL release and adenylate cyclase activity. An inhibitory guanyl nucleotide component may link the mu-opiate receptor to adenylate cyclase.
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PMID:A mu-opiate receptor in 7315c tumor tissue mediates inhibition of immunoreactive prolactin release and adenylate cyclase activity. 609 35

1. The effects were studied of vasoactive intestinal polypeptide (VIP), theophylline, and morphine on net water flux and cyclic adenosine 3',5'-monophosphate (cyclic AMP) levels in the jejunum of anaesthetized rats in vivo and of VIP and morphine on adenylate cyclase activity in rat epithelial cell membranes in vitro. 2. Infusion of VIP (0.1-2 x 10(-9) mol/min/kg) dose dependently caused a reversal from net water absorption to net secretion; 2 x 10(-9) mol/min/kg enhanced the mucosal cyclic AMP content by 67%. 3. Theophylline (5 mg/ml, intraluminally) enhanced the effect of intra-arterial infusion of VIP (2 x 10(-9) mol/min/kg) as to net water secretion and increase in mucosal cyclic AMP content. 4. Pretreatment with morphine (5 mg/kg, s.c.) did not influence the effects of VIP on net water flux and on mucosal cyclic AMP content. 5. Atropine (2 mg/kg, s.c.) also failed to reduced the effect of VIP (0.4 x 10(-9) mol/min/kg) on net water flux. 6. Stimulation of adenylate cyclase activity was a function of VIP concentration over a range of 1 x 10(-10)-1 x 10(-7) M. Morphine (up to 1 x 10(-3) M) failed to influence stimulation of adenylate cyclase by VIP. 7. The finding that low doses of VIP, which already have an effect on net water flux, fail to increase cyclic AMP levels makes it likely that other mediators besides cyclic AMP are involved in the effect of VIP on net water flux. Some of the present results, however, support the assumption that VIP stimulates intestinal fluid secretion by increasing mucosal cyclic AMP levels.
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PMID:Influence of vasoactive intestinal polypeptide on net water flux and cyclic adenosine 3',5'-monophosphate formation in the rat jejunum. 625 42

Morphine inhibited the adenylate cyclase activity of the crude synaptosomal fraction of the rat caudate nucleus in the presence of BTP, GDP, Gpp(NH)p or ITP. The purine nucleotides themselves had an inhibitory action on the enzyme. Beta-endorphin and Met-enkephalin also inhibited the enzyme in the presence of GTP. The GTP-dependent in inhibitory action of morphine was blocked by naloxone. Various opiates and opioid peptides inhibited the enzyme by up to approximately 20 per cent in the presence of GTP. The relative potency was in higher order of levorphanol greater than beta-endorphin greater than Met-enkephalin greater than morphine greater than pentazocine. Levorphanol was about 50,000 times as potent as its biologically inactive enantiomer, dextrorphan. Morphine enhanced the inhibitory actions of GTP and GTPase-resistant Gpp(NH)p on the adenylate cyclase activity. These results suggest that GTP plays an important role in the regulation of adenylate cyclase activity in the rat caudate nucleus and that the occupation of opiate receptor by agonists inhibits the enzyme through an actual increase in the inhibitory action of GTP, rather than a suppression of the enzymatic degradation of GTP.
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PMID:Inhibition of adenylate cyclase by GTP and its modulation by opiate receptor in rat caudate nucleus. 627 23

The effects of morphine on plasma cyclic nucleotide levels and on locomotor activity were investigated in four inbred strains of male mice. Morphine increased both cyclic AMP and cyclic GMP levels as well as locomotor activity in C57BL/6N mice. In BALB/cAnN mice, morphine increased plasma cyclic GMP levels and motor activity without changes in plasma cyclic AMP levels. In C3H/HeN mice, morphine increased plasma cyclic GMP levels without changing cyclic AMP levels and motor activity, but neither plasma cyclic nucleotide levels nor motor activity were increased by morphine in DBA/2N mice. Epinephrine and carbachol increased plasma cyclic AMP and cyclic GMP levels, respectively, in both C57BL and DBA mice. These results show that there is a significant strain difference in the effects of morphine on plasma cyclic nucleotide levels as well as motor activity. The major cause of strain difference in the effects of morphine on cyclic nucleotide levels is unlikely to be due to the difference in the regulation of adenylate cyclase linked to adrenoceptors or that of guanylate cyclase connected with cholinoceptors.
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PMID:Strain difference in morphine-induced increase in plasma cyclic AMP and cyclic GMP levels in relation to locomotor activity in male mice. 628 69

The adenylate cyclase in two particulate preparations from rat brain, a homogenate from caudate nucleus (CN-homogenate) and a synaptosomal plasma membrane fraction (SPM-fraction) from whole rat brain was investigated. Stimulation of the enzyme by dopamine and prostaglandins E1 and E2 was found in the CN-homogenate while only a weak prostaglandin E1 and E2 stimulation and no dopamine stimulation could be found in the SPM-fraction. Guanyl-5'-yl-imidophosphate (GppNHp) and NaF could stimulate the adenylate cyclase in both preparations. Morphine up to 10(-5) M altered neither the basal enzyme activity nor any of the stimulated enzyme activities.
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PMID:Adenylate cyclase in rat synaptosomal plasma membranes and caudate nucleus homogenate: effects of dopamine, E prostaglandins, guanyl-5'-yl-imidodiphosphate and morphine. 628 4

Morphine (10 mg/kg s.c.) was shown to increase net basal water and electrolyte absorption in rat ileum and colon perfused in vivo. These effects were significantly greater in the ileum. Under the same conditions of dosage and time course of administration the activities of relevant mucosal enzymes were studied. Ileal mucosal adenylate cyclase stimulated by prostaglandin E2 (PGE2) in vitro was inhibited by morphine pretreatment. Colonic stimulated cyclase activity was unaffected as were basal activities in both regions. Morphine did not alter the activities of enzymes involved in PGE2 metabolism and is unlikely to act by modulating endogenous PG levels. Transport ATPase activities, were also unchanged in morphine treated animals. These results are discussed in relation to the mechanism of action of morphine on intestinal mucosa.
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PMID:Effects of morphine on net water absorption, mucosal adenylate cyclase activity and PGE2 metabolism in rat intestine. 629 27

A study was made of the effect of morphine on the cAMP level in peripheral blood lymphocytes in tobacco smoking and non-smoking donors. Morphine was shown to produce the naloxone-removable activation of adenylate cyclase, the relationship between enzymatic activity and opiate concentration in the medium being complex in nature. In tobacco smoking donors, the maximal effect on cAMP was produced by morphine at concentrations that were one order of magnitude higher than those in non-smoking ones. On the basis of the data obtained the assumptions are made (1) about the presence on the lymphocytes of opiate receptors whose action mode is associated with adenylate cyclase control, and (2) about the development during tobacco smoking of morphine tolerance at the level of opiate-dependent adenylate cyclase of lymphocytes.
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PMID:[Effect of morphine on the cAMP level of lymphocytes]. 630 38

Adenosine, 2-chloroadenosine and prostaglandin E1 which are known to increase cyclic AMP in neuroblastoma cells potentiated the acetylcholine-induced muscarinic hyperpolarization of the cells without changing the resting membrane potential. The potentiation caused by 2-chloroadenosine was further augmented by Ro 20-1724, a phosphodiesterase inhibitor. A direct intracellular pressure application of cyclic AMP potentiated the muscarinic hyperpolarization without changing the resting membrane potential. Morphine which inhibits adenylate cyclase antagonized 2-chloroadenosine-induced potentiation of the muscarinic hyperpolarization. These results suggest that changes in cyclic AMP level modulate the muscarinic response of neuroblastoma cells.
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PMID:Cyclic AMP-mediated potentiation of muscarinic hyperpolarization in neuroblastoma cells. 632 Sep 77

To elucidate a possible mechanism whereby opiates affect human intestinal fluid secretion, opiate effects on human basal and stimulated colonic adenylate cyclase activity were determined. Morphine (10 microM) and naloxone (1 microM) did not affect basal colonic adenylate cyclase activity: 32.6 +/- 2.6 (n = 23; X +/- S.E.) pmol cAMP/mg protein per 10 min or its stimulation induced by sodium fluoride or VIP. However, morphine inhibited the stimulation induced by prostaglandin E2, an effect which was blocked by naloxone. Synthetic enkephalins and metabolically stable retro inverso enkephalins also prevented PGE2-induced stimulation of colonic adenylate cyclase activity. The addition of calcium (0.1 mM) decreased the basal and PGE2-stimulated enzyme activities by 35% and 50%, respectively, regardless of the presence or absence of morphine. These results suggest that morphine and synthetic enkephalins do not affect basal human colonic adenylate cyclase activity but inhibit its stimulation induced by PGE2. This effect may be one of the mechanisms whereby opiates affect intestinal fluid transport.
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PMID:Effect of opiates on human colonic adenylate cyclase activity. 658 Jan 73


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