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:4.6.1.2 (guanylate cyclase)
8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium nitroprusside effected a rapid, dose-dependent increase in intracellular cGMP accumulation in freshly dispersed bovine parathyroid cells. The effect was half-maximal between 10(-4) and 3 X 10(-4)M, maximal at 3 X 10(-3)M nitroprusside and could be amplified (approximately 50%) by the addition of methylisobutylxanthine (4 X 10(-4)M). The dose-response characteristics were similar to those previously described for the inhibition of cAMP accumulation and PTH release by this agent. Neither dibutyryl cGMP (10(-3)M) nor 8'-bromo-cGMP (10(-3)M) mimicked the inhibitory effect of nitroprusside on cAMP accumulation or PTH release. Dose-dependent stimulation of guanylate cyclase was found in a particulate preparation of parathyroid cells; activity was maximal at 10(-4)M nitroprusside while higher concentrations appeared to inhibit the enzyme. Nitroprusside significantly reduced both (-)isoproterenol and guanine nucleotide-stimulated adenylate cyclase activity in the particulate preparation with maximum inhibition between 10(-3)-10(-2)M. cGMP concentrations as high as 10(-4)M did not affect agonist-stimulated cAMP synthesis. Thus, although the kinetic and dose-response characteristics of the nitroprusside effect on cGMP suggest a linkage to its previously described effects on cAMP and PTH secretion, no direct evidence was found to indicate a causal relationship between the two. Rather it would appear that the effects on the adenylate and guanylate cyclase enzymes occur in parallel, possibly the result of some common primary perturbation of cellular physiology.
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PMID:Sodium nitroprusside inhibition of parathyroid hormone release is not mediated through cyclic GMP. 611 8

Phospholipid composition of Tetrahymena plasma membranes was modified by phospholipase A2-treatment and its effects on the activities of the two membrane-bound cyclases (adenylate and guanylate) were studied. Phospholipase A2 from Crotalus adamanteus was found to hydrolyze preferentially phosphatidylethanolamine of isolated plasma membranes. In the phospholipase A2-treated membranes in which 45% of total phosphatidylethanolamine was converted to its lysolipid, adenylate cyclase activity was to a small extent reduced, whereas guanylate cyclase activity was decreased almost to a half. However, the stimulation rate of the guanylate cyclase activity by calmodulin was unaffected in phospholipase A2-treated plasma membranes. The apparent Km value for substrates was not different between phospholipase A2-untreated and -treated plasma membranes. The ESR analysis demonstrated that the phospholipase A2-treated plasma membranes showed an increased fluidity in the range above 25 degrees C as compared to the untreated control membranes. These results suggest that guanylate cyclase is more dependent on phospholipid environment than adenylate cyclase in Tetrahymena plasma membranes, presumably offering evidence for the different location of two enzymes in the membrane.
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PMID:Differential inhibitory effects by phospholipase A2 on guanylate and adenylate cyclases of Tetrahymena plasma membranes. 612 36

The content of cyclic nucleotides and the activity of adenylate and guanylate cyclases as well as of cAMP phosphodiesterase in the human hyperplastic adrenals were determined after one- and two-step bilateral adrenalectomy for Itsenko-Cushing's disease. A decrease in cGMP concentration and a corresponding increase in cAMP/cGMP correlation were seen in the 2nd hyperplastic adrenal comparatively to those in the 1st one. An enhanced basal activity of adenylate cyclase and its lowered sensitivity to ACTH were found in the 1st and the 2nd adrenals. These changes correlate with a rise in the blood ACTH concentration in patients after the ablation of one adrenal. It is suggested that the augmented adenylate cyclase activity leads to an increased activation of steroidogenesis enzymes in the rest adrenal, ensuring the elevated rate of corticosteroid secretion. The nature of changes in guanylate cyclase activity is contrary to that of adenylate cyclase; namely, guanylate cyclase basal activity of the 2nd hyperplastic adrenal was shown to be lower than that of the 1st one. The cAMP phosphodiesterase activity in the 1st and the 2nd adrenals remained unchanged.
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PMID:[Adenylate and guanylate cylase system function in human hyperplastic adrenals in Itsenko-Cushing disease]. 614 97

Stimulant action of the mitogenic polyanion, polyacrylic acid (PAA) was investigated in mouse lymphocyte culture in vitro. B cell division was induced by "impulsive" PAA treatment. Shortly after PAA treatment the activity of the membrane enzymes, adenylate and guanylate cyclases, was assayed according to the changes in the concentration of cAMP and cGMP. The effect of PAA on the time course of cAMP and cGMP in lymphocytes was compared to the effect of B cell mitogen of other chemical nature--bacterial lipopolysaccharide (LPS). PAA was demonstrated to produce no effect on the activity of membrane cyclase enzymes. On the contrary, following LPS addition guanylate cyclase in the lymphocyte membrane was activated within the first 5-10 minutes. Later on (after 2h) the cells activated with LPS showed an increase in adenylate cyclase activity. By the 12th-24th hour the concentration of cAMP in the LPS-stimulated cells reached 250% of the control level. The differences are discussed between the mitogenic polyanion (PAA) and the lipid-modifying mitogen (LPS) in the molecular mechanisms by which the lymphocyte responses are activated.
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PMID:[Analysis of the cyclase enzyme activity of the cell membrane following lymphocyte stimulation with a mitogenic polyanion]. 614 37

An examination of the effects of 250 or 1500 micrograms m-3 concentrations of diesel particulate from diesel exhaust on the activity of adenylate or guanylate cyclase was undertaken using liver and lung tissue of rats and guinea pigs. These membrane and cytosolic enzymes were selected to screen for functional or regulatory alterations in these tissues. The studies for adenylate cyclase used the microsomal membrane fraction of each tissue; for guanylate cyclase, the microsomal membrane and supernate fractions were used. Basal and fluoride-stimulated adenylate cyclase activity were measured. Basal and sodium azide-stimulated guanylate cyclase activity were also determined. The basal activity of rat liver adenylate cyclase is generally unchanged throughout 52 weeks of diesel exposure. Stimulated adenylate cyclase shows an age-related decrease for all animal treatments throughout the study. Changes in enzyme activity occurred at 12 weeks and 52 weeks after 1500 micrograms m-3 exposure. Soluble stimulated guinea pig lung guanylate cyclase was first increased (6 weeks) and then decreased (24 weeks) by diesel exposure. At 52 weeks, there was no change. The data suggest the following trends: (1) an increased basal adenylate cyclase in the rat lung; (2) an age-related decrease in adenylate cyclase activity in rat liver, and (3) a biphasic exposure-related response of soluble guanylate cyclase for the guinea pig lung during the first 24 weeks, but no change at 52 weeks. In general, however, these studies suggest that diesel exposure does not substantially alter either of these intracellular regulating enzymes.
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PMID:Effect of diesel particulate exposure on adenylate and guanylate cyclase of rat and guinea pig liver and lung. 614 72

The mast cell is the cellular basis for immediate hypersensitivity reactions. The specificity of the immediate hypersensitivity reaction is attributable to IgE molecules fixed to specific membrane receptors which, when stimulated by specific antigen, initiates the process of degranulation of the mast cell. The granules provide three separate sources of biologic activity: performed or primary mediators, newly generated or secondary mediators, and activities associated with the granular matrix. A number of biologic consequences are generated in response to these mediators and these include: increased vascular permeability, vasodilation, smooth muscle spasm, polymorphonuclear leukocyte chemotaxis, stimulation of adenylate and guanylate cyclase, superoxide radical generation, prostaglandin formation, mucous and gastric acid secretion, hypotension, tissue destruction, and mononuclear leukocyte infiltration. This pharmacopia of activities accounts for the clinical aspects of allergic diseases, suggests that the mast cell granule may be involved in the host's defense against parasitic infections, and is compatible with a suggested role of the mast cell as a widely distributed, monocellular endocrine system.
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PMID:The mast cell. 617 51

The purpose of this study is to define the hormonal regulation of pulmonary surfactant secretion in two models, the isolated perfused rat lung and the isolated alveolar type II cell in culture. In the perfused lung, both cholinergic and adrenergic stimulation independently increased labeled disaturated phosphatidylcholine secretion, the major phospholipid component of surfactant, each by 2.3-fold. A concomitant increase in lung cGMP and cAMP concentration of 275- and 25-fold, respectively, was observed. The effect of each agonist was inhibited only by its appropriate antagonist. In alveolar type II cells in culture, both adenylate and guanylate cyclase responded to their appropriate agonists and antagonists. The release of 3H-labeled disaturated phosphatidylcholine was enhanced by beta-adrenergic but not alpha-adrenergic or cholinergic agonists. The effect of isoproterenol (10 microM) on surfactant release was seen by 2.5 min, and secretion was stimulated 2.9-fold at a half-maximal concentration of 1 nM. Cyclic AMP levels were increased by 4.9-fold by isoproterenol at a half-maximal concentration of 40 nM. These results indicate that while in the perfused lung, secretion is stimulated by both adrenergic and cholinergic effectors, in the type II cell model, surfactant secretion is under only beta-adrenergic control.
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PMID:Adrenergic and cholinergic regulation of lung surfactant secretion in the isolated perfused rat lung and in the alveolar type II cell in culture. 625 57

A great deal of knowledge has been gained concerning the activation of adenylate and guanylate cyclase in epidermal cells. Adenylate cyclase is activated by 4 different independent receptors-responding respectively to catecholamine (beta), to prostaglandins (E), to histamine (H2), and to adenosine and it phosphorylated derivatives. Upon activation, each of these receptors becomes unresponsive to further stimulation by its specific stimulator. Guanylate cyclase, on the other hand, is activated by histamine (H1) and epidermal growth factor (EGF). Unlike EGF, the histamine activation is extremely rapid (less than 5 minutes). Epidermal cells are permeable (leak) to cyclic GMP but not cyclic AMP. When the skin is traumatized or injured in any way (even by intradermal injection) there is a sudden catastrophic change in the intracellular levels of the cyclic nucleotides (and of ATP). Cyclic AMP rapidly rises to perhaps 5-10 times its normal resting level while cyclic GMP falls to 10-20% of its level in vivo. The rise in cyclic AMP is due to activation of adenylate cyclase while the fall in cyclic GMP is due in major part to activation of cyclic GMP phosphodiesterase (and perhaps the fall in ATP is due to activation of ATPase). The changes in ATP and cyclic AMP can be reversed by incubating the tissue in a buffered salt solution containing glucose, but this does not normalize the cyclic GMP content. The fall in cyclic GMP can be prevented by a phosphodiesterase inhibitor (IBMX ). This series of events has been called the "ischemia effect." However, it implies that a lack of oxygen is at fault, and that has not been shown to be the case. Its underlying cause and possible physiologic significance are not known. Do these changes in cyclic nucleotides have effects on epidermal proliferation? And does EGF? Agents which increase cyclic AMP do inhibit the epidermal outgrowth and mitotic activity of explant cultures of pig skin. Cyclic GMP does increase outgrowth at a particular concentration. Histamine, which elevates both cyclic nucleotides, has a biphasic action depending on its concentration. These findings imply that these nucleotides do act as one of the controls of epidermal proliferation. The action of cyclic GMP is not accompanied by detectably increased phosphorylation of epidermal proteins. On the other hand, EGF action which also enhances epidermal outgrowth is characterized by an increased protein phosphorylation that precedes any increase in cellular cyclic GMP. We conclude that the action of EGF is independent of the cyclic nucleotide system.
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PMID:Cyclic GMP system in the epidermis. 626 50

In rabbit ileum in vitro Clostridium difficile toxin (200 microliter crude extract) almost abolished net Na absorption, by decreasing mucosa to serosa flux, and induced net Cl secretion by increasing the serosa to mucosa flux. These flux changes were induced when there was no visible histological damage to the mucosa. The toxin did not influence adenylate or guanylate cyclase activity in a plasma membrane fraction of isolated rabbit enterocytes nor did it affect cAMP concentrations in intact rabbit ileum pre-incubated with toxin. The flux responses to the toxin were prevented by removing calcium from the serosal medium, suggesting that the secretory process may be calcium dependent. These results indicate a possible mechanism by which this toxin could induce diarrhoea.
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PMID:Clostridium difficile toxin-induced intestinal secretion in rabbit ileum in vitro. 630 15

Hypertension and atherosclerosis are associated with structural and functional changes that may be collectively described as a 'sick vessel syndrome'. Structural changes in blood vessels (remodelling and hypertrophy) may be protective and adaptive. Functional changes in blood vessels include impairment of endothelium-dependent relaxation and impaired relaxation in response to activation of ATP-sensitive potassium channels. In general, vasorelaxation in response to direct activation of adenylate and guanylate cyclase is preserved in chronic hypertension and atherosclerosis. Vasoconstrictor responses to selected stimuli, such as serotonin, may be greatly potentiated. Impairment of endothelial function in combination with exaggeration of vasoconstrictor responses may predispose to vasospasm particularly during atherosclerosis.
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PMID:Sick vessel syndrome: vascular changes in hypertension and atherosclerosis. 747 26


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