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 incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1-14 C] stearic, [1-14 C] linoleic or [1-14 C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10(-5) M adrenaline and 10(-7) M adenosine. The alpha-agonist phenylephrine and the beta-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.
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PMID:Adrenaline stimulation of phospholipid metabolism in adipocyte ghosts. 345 41

Synergistic interaction between ADP, adrenaline, 5-hydroxytryptamine (5HT) and [8-arginine]vasopressin is not observed for the aggregatory response of aspirin-treated human platelets when this response is estimated directly from the decrease in the number of single platelets in the suspension. This finding is in marked contrast with prior reports of synergistic interaction between these agonists when the rate and extent of the aggregometer response is estimated from the increase in the light transmittance of the suspension, using a platelet aggregometer. We propose that the apparent synergistic response detected using the aggregometer results from the inability of this instrument to respond during the initial phase of aggregation. Significant synergistic interaction is observed for the increase in cytosolic [Ca2+] induced by addition of the ADP/5HT and, to a lesser extent, of the ADP/vasopressin agonist pairs as compared with that caused by addition of the individual agonists. This effect is not, however, typical of the system since increases in cytosolic [Ca2+] induced by addition of the ADP/thrombin or 5HT/vasopressin agonist pairs are no greater than the sum of the responses to these agonists added separately. Addition of collagen prior to ADP or 11,9-epoxymethanoprostaglandin H2 (U46619) fails to enhance the increase in cytosolic [Ca2+] induced by these latter agonists. Adrenaline, when added prior to non-saturating concentrations of U46619, thrombin, vasopressin or ADP, significantly enhances the increase in cytosolic [Ca2+] induced by these agonists in platelets suspended in media containing less than 0.1 microM or 1 mM Ca2+. However, adrenaline fails to enhance the increase in cytosolic [Ca2+] induced by the divalent cation ionophore, ionomycin. Enhancement by adrenaline of Ca2+ influx induced by U46619, thrombin and ADP has been shown by using Mn2+ as probe. Adrenaline also enhances the extent of [3H]5HT secretion induced by U46619, thrombin and vasopressin but fails to increase that induced by ADP in this aspirin-treated preparation. These results are in part consistent with the postulate that adrenaline, acting via an alpha 2-adrenoceptor, modulates receptor--phospholipase-C coupling. However, such modulation does not appear to involve inhibition of adenylate cyclase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synergistic responses in human platelets. Comparison between aggregation, secretion and cytosolic Ca2+ concentration. 349 Sep 77

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

The effect of dopamine on adenylate cyclase activity was investigated in slices of human term placentas. Dopamine elicited a dose-dependent stimulation of cAMP formation with a ED50 value of about 1 X 10(-6)M dopamine and an increase of 110% over the control with 1 X 10(-4)M dopamine. (-)-Epinephrine and (-)-norepinephrine also increased placental cAMP formation. Apomorphine displayed a slight but non-significant stimulatory effect while bromocriptine was not effective. SCH 23390, a selective antagonist of dopamine D1 receptors caused a dose-dependent decrease of the dopamine activation. In contrast, the dopamine increase of cAMP was unaffected by beta- and alpha-adrenergic blocking drugs and by the D2 selective antagonist, (-)-sulpiride. These data indicate that dopamine stimulates cAMP formation in human term placenta through a specific mechanism via D1 dopaminergic receptors positively coupled to adenylate cyclase.
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PMID:Dopamine-stimulated adenylate cyclase in human term placenta. 377 46

Adenylate cyclase activity of the washed particles from the ventricles of rats made hypothyroid by propylthiouracil (P.T.U.) treatment was studied in the absence or presence of different concentrations of catecholamines, guanylimido-diphosphate (GppNHp) and NaF. The washed particles preparation of hypothyroid rat displayed higher basal adenylate cyclase activity in comparison to that in the euthyroid animal. Fluoride stimulation was unaltered but GppNHp stimulation was markedly depressed over a wide range of concentrations in the hypothyroid heart washed particles. Epinephrine stimulation in the presence of GppNHp was altered only at 10(-5) to 10(-4)M concentrations. Depressed responsiveness of cardiac adenylate cyclase to GppNHp and epinephrine was also found in washed particles of thyroidectomized rats. Depression of GppNHp or epinephrine response in hypothyroid animals was reversed 48 hours after T3 administration. In contrast to the washed particulate preparation, no depressions in the responses of adenylate cyclase to GppNHp or epinephrine were seen in the purified sarcolemmal membranes from P.T.U. induced hypothyroid or thyroidectomized rat hearts. It is proposed that altered guanine nucleotide binding or altered guanine nucleotide binding protein-catalytic subunit interaction in the adenylate cyclase system may be an underlying mechanism of depressed positive inotropic action of catecholamines in the hypothyroid state.
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PMID:Alterations in the cardiac adenylate cyclase activity in hypothyroid rat. 385 Jul 75

Platelets were briefly fixed in paraformaldehyde/glutaraldehyde and then incubated with 5'-adenylyl imidodiphosphate under conditions suitable for the cytochemical detection of adenylate cyclase activity. The adenylate cyclase activity of these platelets retains the ability to respond to prostaglandins E1, D2, I2 (prostacyclin), forskolin and fluoride. Sites of stimulated adenylate cyclase activity were localized cytochemically by the reaction of lead with the reaction product imidodiphosphate to form deposits of lead imidodiphosphate that are visible in the electron microscope. Reaction product deposition was seen only in the dense tubule system of human platelets when the incubation medium contained forskolin, prostacyclin, or prostaglandin D2 at concentrations known to stimulate the enzyme in intact platelets. Epinephrine, an antagonist of adenylate cyclase inhibited the cytochemical reaction stimulated by prostacyclin. The fact that the cytochemical reaction was induced by agonists that stimulate the enzyme through two different types of prostaglandin receptors and by forskolin, which acts distal to the receptors, confirms that the method specifically detects adenylate cyclase. The presence of adenylate cyclase in the dense tubules may be significant for the regulation of intracellular Ca2+ and arachidonic acid metabolism by this membrane system.
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PMID:Cytochemical localization of adenylate cyclase in the dense tubule system of human blood platelets stimulated by forskolin, prostacyclin and prostaglandin D2. 389 Sep 60

1. The mechanism of stimulation of cyclic adenosine 3',5'-monophosphate (cyclic AMP) accumulation by adrenaline and ouabain and the effect of Mn(++) substitution for Mg(++) as the metal ion requirement of this system was studied in cell-free preparations of adenyl cyclase from rat brain.2. In the rat cerebral cortex preparation, substitution of Mn(++) for Mg(++) significantly increased cyclic AMP accumulation while significantly inhibiting adenosine triphosphate (ATP) and adenosine diphosphate (ADP) hydrolysis and adenosine 5'-monophosphate (AMP) accumulation. In the synaptic membrane preparation, in the absence of NaF, the highest amount of ATP hydrolysis was obtained in tissue prepared with Mn(++) and incubated with Mg(++); under these conditions cyclic AMP accumulation was equal to that produced under any other condition and significantly higher than that observed in the presence of Mg(++) prepared and Mg(++) incubated tissue.3. Preparation and/or incubation of tissue with Mn(++) significantly reduced phosphodiesterase (PDE) activity compared to that observed in Mg(++) prepared tissue.4. Adrenaline and ouabain both significantly increased cyclic AMP accumulation in the rat cerebral cortex preparation but did not inhibit ATP or ADP hydrolysis. In the synaptic membrane preparation, in the presence of 0.01 mM Ca(++), adrenaline but not ouabain significantly increased cyclic AMP accumulation. Phenoxybenzamine (0.1 mM) and pronethalol (0.1 mM) significantly inhibited adrenaline-induced cyclic AMP accumulation in both these preparations.5. Ouabain and adrenaline both failed to stimulate cyclic AMP accumulation in the presence of Mn(++) prepared and/or incubated tissue.6. Ouabain and adrenaline had no effect on PDE activity in either of these preparations.7. It was concluded that Mn(++) increased cyclic AMP accumulation in part by indirect inhibition of ATP and ADP hydrolysis which provides inhibitors of cyclic AMP destruction, by direct stimulation of adenyl cyclase and by inhibition of cyclic AMP destruction in a way unrelated to nucleotide inhibition of PDE. Adrenaline and ouabain appeared tp stimulate cyclic AMP accumulation in a more direct manner.
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PMID:The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by adrenaline, ouabain and Mn++. 414 40

Hypothalamic extract, containing the releasing factors for anterior pituitary hormones, within minutes stimulated adenyl cyclase activity and adenosine 3':5'-cyclic phosphate (cyAMP) concentrations in rat anterior pituitary in vitro. Cerebral cortical extract was ineffective and hypothalamic extract had no effect on these parameters in posterior pituitary or thyroid. Prostaglandin E(1) also increased adenyl cyclase activity and cyAMP levels in anterior pituitary tissue. Although NaF augmented adenyl cyclase activity, it did not elevate cyAMP. Epinephrine, norepinephrine, histamine, serotonin, dopamine, and vasopressin did not increase either adenyl cyclase or cyAMP. The increased adenyl cyclase and cyAMP produced by hypothalamic extract was associated with greater luteinizing hormone release from anterior pituitary in vitro.
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PMID:Stimulation of anterior pituitary adenyl cyclase activity and adenosine 3':5'-cyclic phosphate by hypothalamic extract and prostaglandin E1. 431 May 17

Epinephrine, norepinephrine, ACTH, and dibutyryl 3',5'-cyclic AMP reduced adipocyte ATP levels during 60 min incubation; glucose displayed a protective effect. The reduction in adipocyte ATP levels could not be attributed solely to: a direct hormone effect, deficiency in metabolic substrate, activation of adenyl cyclase with ATP consumption, loss of adenine nucleotide from the cell or loss of cells during incubation, lipolytic rate per se, or extracellular accumulation of FFA or glycerol. To determine whether intracellular FFA accumulation was a causative factor, intracellular FFA levels were measured during hormone-stimulated lipolysis. This was accomplished by using sucrose-U-(14)C as a marker for the extracellular space to correct for contamination of cells by extracellular albumin-bound FFA. These experiments showed that the fall in adipocyte ATP correlated with FFA saturation of medium albumin and progressive accumulation of FFA within the adipocyte. Furthermore, the protective effect of glucose noted above was associated with a marked reduction in intracellular FFA as compared to the extracellular FFA pool. On the basis of these studies, combined with those in the literature, it is concluded that in vitro effects of lipolytic agents on adipocyte ATP levels are the net result of imparied ATP synthesis (uncoupled oxidative phosphorylation) in the face of normal or augmented ATP consumption.
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PMID:Reduction in adipocyte ATP by lipolytic agents: relation to intracellular free fatty acid accumulation. 432 9

Basal adenyl cyclase activity and its response to epinephrine and glucagon were studied in isolated adipocyte ghosts obtained from fed, starved, refed, and fat-diet-adapted rats. Epinephrine stimulation of adenyl cyclase was significantly increased in fasted rats, but the glucagon response did not change. Rats fasted for 48 hr and refed a high carbohydrate, low fat diet for 48 or 96 hr showed no differences from chow-fed animals in either basal or hormone-stimulated adenyl cyclase activity. Rats adapted to a high fat, low carbohydrate diet showed an initial and transitory increase in basal activity but a progressive loss of epinephrine- and glucagon-stimulated enzyme activities. The loss in hormone responsiveness correlated well with a decrease in hormone-stimulated lipolysis of fat pads and was associated with a significant increase in fat cell diameter.
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PMID:Effects of starvation, refeeding, and fat feeding on adipocyte ghost adenyl cyclase activity. 433 99


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