Cyclic nucleotides (cAMP and cGMP) in the blood plasma of dogs during extracorporeal charcoal hemoperfusion

1982 ◽  
Vol 94 (3) ◽  
pp. 1214-1217
Author(s):  
A. N. Koterov ◽  
A. V. Nikol'skii ◽  
E. F. Romantsev ◽  
L. A. Vernigorova
Keyword(s):  
Blood Plasma ◽  
Cyclic Nucleotides ◽  
Camp And Cgmp ◽  
Charcoal Hemoperfusion

scholarly journals Quantification of cAMP and cGMP analogs in intact cells: pitfals in enzyme immunoassays for cyclic nucleotides

2011 ◽  
Vol 11 (S1) ◽  
Author(s):  
Katharina Werner ◽  
Frank Schwede ◽  
Hans-Gottfried Genieser ◽  
Jörg Geiger ◽  
Elke Butt
Keyword(s):  
Cyclic Nucleotides ◽  
Intact Cells ◽  
Enzyme Immunoassays ◽  
Camp And Cgmp

CO2 and cerebral circulation in newborn pigs: cyclic nucleotides and prostanoids in vascular regulation

1994 ◽  
Vol 266 (4) ◽  
pp. H1494-H1501 ◽  
Author(s):  
H. Parfenova ◽  
M. Shibata ◽  
S. Zuckerman ◽  
C. W. Leffler
Keyword(s):  
Cyclic Nucleotides ◽  
Cerebrovascular Reactivity ◽  
Cyclic Monophosphate ◽  
Cranial Window ◽  
Vascular Regulation ◽  
Newborn Pigs ◽  
Cerebral Vasodilation ◽  
Ly 83583 ◽  
Camp And Cgmp

The role of cyclic nucleotides and prostanoids in cerebrovascular reactivity to increased carbon dioxide was investigated in anesthetized and artificially ventilated newborn pigs equipped with closed cranial windows. Pial arteriolar diameter was measured, and cortical periarachnoid cerebrospinal fluid (CSF) was collected from beneath the cranial window for determination of adenosine 3',5'-cyclic monophosphate (cAMP), guanosine 3',5'-cyclic monophosphate (cGMP), and prostanoids. Progressively increasing arterial PCO2 (PaCO2) from normocapnia (33 +/- 1 mmHg) to hypercapnia (final PaCO2, 83 +/- 2 mmHg) resulted in dose-dependent pial arteriolar dilation and concomitant increases in cAMP, cGMP, and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) in cortical CSF. N omega-methyl-L-arginine, N omega-nitro-L-arginine, N omega-nitro-L-arginine methyl ester, methylene blue, and LY 83583 did not inhibit cerebral vasodilation or the increases in cortical cAMP/cGMP induced by hypercapnia. Indomethacin abolished the vasodilatory response to hypercapnia and attenuated the hypercapnia-induced increases in cAMP and cGMP. Prostacyclin analogues increased both cAMP and cGMP levels in cortical CSF and induced pial arteriolar dilation (iloprost > carbaprostacyclin). The present data suggest that in newborn pigs cyclic nucleotides are involved in cerebral vasodilation in response to hypercapnia via a prostanoid-dependent mechanism.

Injection of guanosine 5'-cyclic monophosphate into heart cells blocks calcium slow channels

1985 ◽  
Vol 248 (5) ◽  
pp. H745-H749 ◽  
Author(s):  
G. Bkaily ◽  
N. Sperelakis
Keyword(s):  
Cyclic Nucleotides ◽  
Action Potentials ◽  
Heart Cells ◽  
Myocardial Cells ◽  
Cyclic Monophosphate ◽  
Intracellular Injection ◽  
Ventricular Cells ◽  
Camp And Cgmp ◽  
Slow Action Potentials

The role of guanosine 5'-cyclic monophosphate (cGMP) in the regulation of the ionic slow channels in heart muscle is less well known than that of adenosine 3,'5'-cyclic monophosphate (cAMP). The effects of intracellular injection of cAMP and cGMP in cultured chick embryonic heart (ventricular) cells by the liposome method were studied. Injection of cAMP into the cells induced spontaneous slow action potentials that could be blocked by verapamil and nifedipine. Injection of cGMP blocked on-going slow action potentials, and this effect was reversed by increasing cAMP. Thus both cAMP and cGMP are involved in the regulation of the slow calcium channels in myocardial cells, and the two cyclic nucleotides are antagonistic.

CGRP and ANF cause relaxation of opossum internal anal sphincter via different mechanisms

1991 ◽  
Vol 260 (5) ◽  
pp. G764-G769 ◽  
Author(s):  
S. Rattan ◽  
C. Moummi ◽  
S. Chakder
Keyword(s):  
Smooth Muscle ◽  
Anal Sphincter ◽  
Cyclic Nucleotides ◽  
Internal Anal Sphincter ◽  
Camp Content ◽  
Calcitonin Gene ◽  
Before And After ◽  
Camp And Cgmp

This investigation examined and compared the role of cyclic nucleotides in the mediation of internal anal sphincter (IAS) relaxation caused by the addition of neuropeptide calcitonin gene-related peptide (CGRP) and atrial natriuretic factor (ANF). The studies were performed in vitro on smooth muscle strips of opossum IAS. The relaxation produced by CGRP and ANF was examined before and after the addition of tetrodotoxin (TTX) (1 x 10(-6)M). At this concentration, TTX did not have any significant effect on the relaxation produced by either CGRP or ANF, suggesting that these peptides act directly on the smooth muscle. Addition of CGRP (3 x 10(-6) M) produced the maximal relaxation and significantly increased cAMP content without changing cGMP. On the other hand, addition of ANF (3 x 10(-6) M) caused a similar fall in IAS tension that was accompanied by a significant elevation in cGMP without any change in cAMP content. The rises in the levels of cyclic nucleotides preceded the onset of fall in the resting tension of IAS. Our results demonstrate that CGRP and ANF relax isolated strips of opossum IAS by their action directly at the smooth muscle and that this relaxation is associated with an increase in cAMP and cGMP, respectively. The studies suggest the presence of both cAMP and cGMP pathways in the IAS and that the relaxation of IAS smooth muscle in response to different peptides may occur via a specific intracellular biochemical pathway.

Reduction of cAMP and cGMP inhibitory effects in human platelets by MRP4-mediated transport

2012 ◽  
Vol 108 (11) ◽  
pp. 955-962 ◽  
Author(s):  
Alessandra Borgognone ◽  
Fabio Pulcinelli
Keyword(s):  
Cyclic Nucleotides ◽  
Cyclic Nucleotide ◽  
Thrombus Formation ◽  
Physiological Mechanism ◽  
Human Platelets ◽  
Inhibitory Effects ◽  
Dense Granules ◽  
Dependent Inhibition ◽  
Novel Target ◽  
Camp And Cgmp

SummaryCyclic nucleotide-dependent inhibition of platelets represents the most important physiological way to limit thrombus formation. cAMP and cGMP increase in platelets as a consequence of prostacyclin and nitric oxide production by endothelial cells and act through PKA and PKG, respectively. The cytosolic concentration of cyclic nucleotides in platelets is regulated by AC- and GC-dependent synthesis and PDE-dependent degradation. In some cells cyclic nucleotides are eliminated also through MRP4/5/8-dependent efflux. As only MRP4 is expressed in platelets, at high levels in dense granules, we determined its role in the elimination of cyclic nucleotides from platelet cytosol. We studied the effects of MRP4 inhibition on cAMP/cGMP effects in platelets. Cyclic nucleotide inhibitory effects triggered by cAMP and cGMP-elevating agents on platelet aggregation are strongly enhanced by MRP4 inhibition and so is cyclic nucleotide-dependent phosphorylation of the common substrate VASP. MRP4 inhibition decreases cAMP concentration in platelet granules and both cAMP and cGMP compete with an established substrate of MRP4 (fluo-cAMP) for entrance in granules. Here we provide the first evidence of the transport of cyclic nucleotides mediated by MRP4 as part of their physiological mechanism of elimination in human platelets, which might represent a novel target to increase cyclic nucleotide-dependent inhibition.

Effect of Δ9 tetrahydrocannabinol on cyclic nucleotides in synchronously dividing Tetrahymena

1981 ◽  
Vol 59 (7) ◽  
pp. 489-493 ◽  
Author(s):  
Selma Zimmerman ◽  
Arthur M. Zimmerman ◽  
Helen Laurence
Keyword(s):  
Cell Cycle ◽  
Nous Avons ◽  
Cyclic Nucleotides ◽  
Cyclic Nucleotide ◽  
Significant Variation ◽  
Experimental Treatment ◽  
Twofold Increase ◽  
Synchronized Cells ◽  
Free Running ◽  
Camp And Cgmp

Cyclic nucleotide levels were determined in division-synchronized Tetrahymena and the effect of Δ9-tetrahydrocannabinol (THC) on the cyclic nucleotide levels was studied. In non-drug-treated division-synchronized cells, there was no statistically significant variation in the level of cAMP and cGMP during the G2 period, preceding the first division. During the free running cell cycle (the interval of time between the first and second synchronous division) the twofold increase in the level of cAMP was statistically significant; however the variation in the level of cGMP was not statistically significant.THC caused a lowering of cAMP and cGMP levels throughout the 4-h experimental treatment. The suppression of cAMP and cGMP levels altered the cyclic nucleotide pattern of the cell cycle. The cAMP pattern was changed particularly in the G2 period preceding the first synchronous division, and immediately after division during the free running cell cycle. THC treatment caused division delays of approximately 8–15 min in the onset of the first and second synchronous division. However, the duration of the free running cell cycle (110–120 min) was unchanged. The suppression of cyclic nucleotide levels resulting from THC treatment is discussed in relation to delays in the division schedule.Nous avons déterminé le taux des nucléotides cycliques chez Tetrahymena se divisant de façon synchrone et nous avons étudié l'effet du Δ9-tétrahydrocannabinol (THC) sur le taux de ces nucléotides cycliques. Dans les cellules non traitées, se divisant de façon synchrone, il n'existe aucune variation statistiquement significative dans les teneurs du cAMP et du cGMP durant la période G2 précédant la première division. Durant le cycle cellulaire sans division (l'intervalle de temps entre la première et la seconde division synchrone), la teneur du cAMP augmente de deux fois, une augmentation statistiquement significative; cependant, la variation du taux du cGMP n'est pas statistiquement significative.

Inhibition of IP3 and IP3-dependent Ca2+ mobilization by cyclic nucleotides in isolated gastric muscle cells

1993 ◽  
Vol 264 (5) ◽  
pp. G967-G974 ◽  
Author(s):  
K. S. Murthy ◽  
C. Severi ◽  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Cyclic Nucleotides ◽  
Muscle Cells ◽  
Dibutyryl Camp ◽  
Main Determinant ◽  
Inositol 1,4,5 Trisphosphate ◽  
Gastric Muscle ◽  
Intact Muscle ◽  
Camp And Cgmp ◽  
Permeabilized Muscle ◽  
Stimulation Of

The mechanisms by which cAMP and cGMP and agents that stimulate one (isoproterenol and nitroprusside) or both cyclic nucleotides (VIP) decrease cytosolic free Ca2+ ([Ca2+]i) and inhibit contraction were examined in dispersed, intact, and saponin-permeabilized gastric muscle cells. In these cells, the [Ca2+]i transient responsible for initial contraction is mediated by inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release (K. N. Bitar, P. G. Bradford, J. W. Putney, Jr., and G. M. Makhlouf, Science Wash. DC 232: 1143-1145, 1986, and J. Biol. Chem. 261: 16591-16596, 1986). In intact muscle cells, dibutyryl cAMP and all three relaxant agents inhibited contraction, [Ca2+]i, and net Ca2+ efflux (i.e., Ca2+ release) in a concentration-dependent fashion. In permeabilized muscle cells, cAMP, cGMP, and all three relaxant agents 1) inhibited cholecystokinin (CCK)-induced IP3 production (maximal 38-48%), 2) inhibited CCK- and IP3-induced Ca2+ efflux (maximal 55-59%) and contraction (maximal 59-66%), and 3) stimulated Ca2+ uptake (maximal 25-30%), in a concentration-dependent fashion. cAMP and cGMP were equipotent inhibitors of IP3 production and of CCK- and IP3-induced Ca2+ efflux and contraction, whereas cGMP was distinctly more potent as a stimulant of Ca2+ uptake. For all functions, maximal effects induced by cAMP and cGMP were similar to those induced by the three relaxant agents. Inhibition of Ca2+ release was the main determinant of inhibition of contraction; stimulation of Ca2+ uptake was relatively minor (< 5% of Ca2+ efflux). Decrease in IP3 production did not contribute to inhibition of Ca2+ efflux and contraction since inhibition of IP3-induced Ca2+ efflux was similar to inhibition of CCK-induced IP3-dependent Ca2+ efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium regulation of GAF domain function

2007 ◽  
Vol 35 (5) ◽  
pp. 1032-1034 ◽  
Author(s):  
M.J. Cann
Keyword(s):  
Cyclic Nucleotides ◽  
Protein Domain ◽  
Genetic Ablation ◽  
Anabaena Pcc 7120 ◽  
Cyanobacterium Anabaena ◽  
Signal Changes ◽  
Sodium Regulation ◽  
Pcc 7120 ◽  
Camp And Cgmp

Cyclic nucleotide PDEs (phosphodiesterases) regulate cellular levels of cAMP and cGMP by controlling the rate of degradation. Several mammalian PDE isoforms possess N-terminal GAF (found in cGMP PDEs, Anabaena adenylate cyclases and Escherichia coli FhlA; where FhlA is formate hydrogen lyase transcriptional activator) domains that bind cyclic nucleotides. Similarly, the CyaB1 and CyaB2 ACs (adenylate cyclases) of the cyanobacterium Anabaena PCC 7120 bind cAMP through one (CyaB1) or two (CyaB2) N-terminal GAF domains and mediate autoregulation of the AC domain. Sodium inhibits the activity of CyaB1, CyaB2 and mammalian PDE2A in vitro through modulation of GAF domain function. Furthermore, genetic ablation of cyaB1 and cyaB2 gives rise to Anabaena strains defective in homoeostasis at limiting sodium. Sodium regulation of GAF domain function has therefore been conserved since the eukaryotic/prokaryotic divergence. The GAF domain is the first identified protein domain to directly sense and signal changes in environmental sodium.

scholarly journals The generation and regulation of lymphocyte populations: evidence from differentiative induction systems in vitro.

1978 ◽  
Vol 147 (6) ◽  
pp. 1727-1743 ◽  
Author(s):  
M P Scheid ◽  
G Goldstein ◽  
E A Boyse
Keyword(s):  
B Cells ◽  
Cyclic Nucleotides ◽  
General Scheme ◽  
Pharmacological Agents ◽  
Inductive Effects ◽  
Camp Induction ◽  
Camp And Cgmp ◽  
Lymphocyte Populations ◽  
Two Populations

Results with a dual assay, for the induction of Thy-1+ T cells and of CR+ B cells from marker-negative precursors, confirm that thymopoietin is at present the only known selective inducer of prothymocytes. In contrast, various inducers, including ubiquitin, are active in both assays. Pharmacological evidence indicates that there are different cellular receptors for ubiquitin and thymopoietin. Prothymocytes and pro-CR+ B cells compose two distinct populations in bone marrow and spleen; their distribution in density gradients is different, and elimination of either population enriches the other proportionately. There are no noteworthy differences between induction of these two populations in regard to (a) kinetics, (b) dependence on temperature and protein synthesis, (c) activation by cAMP, and (d) inhibition by cGMP. The opposite inductive effects of cAMP and cGMP were corroborated by the use of pharmacological agents that raise or lower the levels of intracellular cyclic nucleotides. In contrast, a third induction assay, which monitors acquisition of the PC+ surface phenotype, indicates that this differentiative step, the last known for B cells, is initiated by cGMP and inhibited by cAMP. Induction of PC is also inhibited by thymopoietin, signifying that the inductive selectivity of thymopoietin is not due to restriction of its receptors to the T lineage cells. Rather it seems that receptors for thymopoietin occur also on PC-inducible and other B cells, although in this case geared biochemically to inhibition rather than expression of the succeeding gene program. This suggests a role for thymopoietin in the coordinated interregulation of lymphocyte classes, in addition to its better-known function as the thymic inducer of prothymocytes. Present data conform to a general scheme in which the cyclic nucleotides cAMP and cGMP, and agents that affect intracellular levels of these mediators, influence reciprocally the early and late (functional) phases of lymphocyte differentiation as a whole, while thymopoietin influences reciprocally the differentiation of the B and T classes of lymphocyte.

scholarly journals cAMP and cGMP in nasal mucus related to severity of smell loss in patients with smell dysfunction

2008 ◽  
Vol 31 (2) ◽  
pp. 78 ◽  
Author(s):  
R I Henkin ◽  
I Velicu
Keyword(s):  
Cyclic Nucleotides ◽  
Type I ◽  
Type Ii ◽  
Systematic Classification ◽  
Type Iii ◽  
Nasal Mucus ◽  
Camp And Cgmp ◽  
Taste And Smell ◽  
Loss Severity ◽  
Smell Loss

Purpose: To evaluate nasal mucus levels of cAMP and cGMP in patients with taste and smell dysfunction with respect to severity of their smell loss. Methods: cAMP and cGMP were measured in nasal mucus using a sensitive spectrophotometric 96 plate ELISA technique. Smell loss was measured in patients with taste and smell dysfunction by standardized psychophysical measurements of olfactory function and classified by severity of loss into four types from most severe to least severe such that anosmia > Type I hyposmia > Type II hyposmia > Type III hyposmia. Measurements of nasal mucus cyclic nucleotides and smell loss were made independently. Results: As smell loss severity increased stepwise cAMP and cGMP levels decreased stepwise [cAMP, cGMP (in pmol/ml); anosmia – 0.004, 0.008: Type I hyposmia – 0.12±0.03, 0.10±0.03: Type II hyposmia – 0.15±0.02, 0.16±0.01: Type III hyposmia – 0.23±0.05, 0.20±0.15]. Conclusions: These results confirm the association of biochemical changes in cyclic nucleotides with systematic losses of smell acuity. These results confirm the usefulness of the psychophysical methods we defined to determine the systematic classification of smell loss severity. These changes can form the basis for the biochemical definition of smell loss among some patients with smell loss as well as for their therapy.

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