Academic literature on the topic 'CAMP/cGMP'

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Journal articles on the topic "CAMP/cGMP"

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Jiang, Hang, John B. Shabb, and Jackie D. Corbin. "Cross-activation: overriding cAMP/cGMP selectivities of protein kinases in tissues." Biochemistry and Cell Biology 70, no. 12 (1992): 1283–89. http://dx.doi.org/10.1139/o92-175.

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cAMP- and cGMP-dependent protein kinases are homologous proteins and are predicted to exhibit very similar three-dimensional structures. Their cyclic nucleotide binding domains share a high degree of amino acid sequence identity. cAMP- and cGMP-dependent protein kinases are activated relatively specifically by cAMP and cGMP, respectively; and a single alanine–threonine difference between cAMP- and cGMP-binding domains partially accounts for this specificity. Thus, it would be expected that cAMP and cGMP mediate separate physiological effects. However, owing in part to the lack of absolute spec
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Inamura, Kouhei, Makoto Kashiwayanagi, and Kenzo Kurihara. "Effects of cGMP and sodium nitroprusside on odor responses in turtle olfactory sensory neurons." American Journal of Physiology-Cell Physiology 275, no. 5 (1998): C1201—C1206. http://dx.doi.org/10.1152/ajpcell.1998.275.5.c1201.

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The effects of cGMP and sodium nitroprusside (SNP) on odor responses in isolated turtle olfactory neurons were examined. The inward current induced by dialysis of a mixture of 1 mM cAMP and 1 mM cGMP was similar to that induced by dialysis of 1 mM cAMP or 1 mM cGMP alone. After the neurons were desensitized by the application of 1 mM cGMP, 3 mM 8-(4-chlorophenylthio)-cAMP, a membrane-permeable cAMP analog, did not elicit any current, indicating that both cAMP and cGMP activated the same channel. Extracellular application of SNP, a nitric oxide (NO) donor, evoked inward currents in a dose-depen
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Xu, Hao-Liang, Hailemariam M. Wolde, Vitaliy Gavrilyuk, Verna L. Baughman, and Dale A. Pelligrino. "cAMP modulates cGMP-mediated cerebral arteriolar relaxation in vivo." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 6 (2004): H2501—H2509. http://dx.doi.org/10.1152/ajpheart.00319.2004.

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No studies have specifically addressed whether cAMP can influence nitric oxide (NO)/cGMP-induced cerebral vasodilation. In this study, we examined whether cAMP can enhance or reduce NO-induced cerebral vasodilation in vivo via interfering with cGMP efflux or through potentiating phosphodiesterase 5 (PDE5)-mediated cGMP breakdown, respectively, in cerebral vascular smooth muscle cells (CVSMCs). To that end, we evaluated, in male rats, the effects of knockdown [via antisense oligodeoxynucleotide (ODN) applications] of the cGMP efflux protein multidrug resistance protein 5 (MRP5) and PDE5 inhibit
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Hasegawa, K., H. Kikuchi, S. Ishizaki, et al. "Simple fluctuation of Ca2+ elicits the complex circadian dynamics of cyclic AMP and cyclic GMP in Paramecium." Journal of Cell Science 112, no. 2 (1999): 201–7. http://dx.doi.org/10.1242/jcs.112.2.201.

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The circadian dynamics of cyclic adenosine 3′,5′-monophosphate (cAMP) and cyclic guanosine 3′,5′-monophosphate (cGMP) were simulated in Paramecium multimicronucleatum. The mathematical functions determined closely mimic the Ca2+ dependence of adenylate cyclase (AC) and guanylate cyclase (GC) activities as documented in P. tetraurelia. Patterns of cAMP concentration ([cAMP]), cGMP concentration ([cGMP]), and the ratio [cGMP]/[cAMP] were calculated with respect to Ca2+ concentrations ([Ca2+]) fluctuating sinusoidally with a period of 24 hours at three different levels: low, medium, and high. The
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Stangherlin, Alessandra, and Manuela Zaccolo. "cGMP–cAMP interplay in cardiac myocytes: a local affair with far-reaching consequences for heart function." Biochemical Society Transactions 40, no. 1 (2012): 11–14. http://dx.doi.org/10.1042/bst20110655.

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cAMP and cGMP signalling pathways are common targets in the pharmacological treatment of heart failure, and often drugs that modulate the level of these second messengers are simultaneously administered to patients. cGMP can potentially affect cAMP levels by modulating the activity of PDEs (phosphodiesterases), the enzymes that degrade cyclic nucleotides. This biochemical cross-talk provides the means for drugs that increase cGMP to concomitantly affect cAMP signals. Recent studies using FRET (fluorescence resonance energy transfer) reporters and real-time imaging show that, in cardiac myocyte
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DICKINSON, Natalie T., Elliott K. JANG, and Richard J. HASLAM. "Activation of cGMP-stimulated phosphodiesterase by nitroprusside limits cAMP accumulation in human platelets: effects on platelet aggregation." Biochemical Journal 323, no. 2 (1997): 371–77. http://dx.doi.org/10.1042/bj3230371.

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cGMP enhances cAMP accumulation in platelets via cGMP-inhibited phosphodiesterase (PDE3) [Maurice and Haslam (1990) Mol. Pharmacol. 37, 671–681]. However, cGMP might also limit cAMP accumulation by activating cGMP-stimulated phosphodiesterase (PDE2). We therefore evaluated the role of PDE2 in human platelets by using erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) to inhibit this enzyme selectively. IC50 values for the inhibition of platelet PDE2 by EHNA, with 10 μM cAMP as substrate in the absence and in the presence of 1 μM cGMP, were 15 and 3 μM respectively. Changes in platelet cyclic [3H]nucl
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Dembinsky, A., H. Rubin, and S. Ravid. "Chemoattractant-mediated increases in cGMP induce changes in Dictyostelium myosin II heavy chain-specific protein kinase C activities." Journal of Cell Biology 134, no. 4 (1996): 911–21. http://dx.doi.org/10.1083/jcb.134.4.911.

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Myosin II heavy chain (MHC)-specific protein kinase C (MHC-PKC) isolated from the ameba, Dictyostelium discoideum, regulates myosin II assembly and localization in response to the chemoattractant cAMP (Abu-Elneel et al. 1996. J. Biol. Chem. 271:977- 984). Recent studies have indicated that cAMP-induced cGMP accumulation plays a role in the regulation of myosin II phosphorylation and localization (Liu, G., and P. Newell. 1991. J. Cell. Sci. 98: 483-490). This report describes the roles of cAMP and cGMP in the regulation of MHC-PKC membrane association, phosphorylation, and activity (hereafter t
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Krizhanovsky, Valery, Orly Agamy, and Michael Naim. "Sucrose-stimulated subsecond transient increase in cGMP level in rat intact circumvallate taste bud cells." American Journal of Physiology-Cell Physiology 279, no. 1 (2000): C120—C125. http://dx.doi.org/10.1152/ajpcell.2000.279.1.c120.

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Initial sweet taste transduction is expected to occur in the subsecond time range. We demonstrate a rapid and transient (75–250 ms) increase of cGMP (but not cAMP) level in rat intact circumvallate taste cells after stimulation by sucrose. This rapid increase does not occur in nonsensory epithelial cells. Pretreatment with a nonspecific phosphodiesterase (PDE) inhibitor (IBMX), a specific cAMP-PDE4 inhibitor (denbufylline), or an adenylyl cyclase activator (forskolin) all increased basal cAMP and abolished the sucrose-stimulated cGMP increase at 150 ms. Pretreatment with a soluble guanylyl cyc
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Segal, J. "Opposite regulatory effects of cAMP and cGMP on sugar uptake in rat thymocytes." American Journal of Physiology-Endocrinology and Metabolism 252, no. 5 (1987): E588—E594. http://dx.doi.org/10.1152/ajpendo.1987.252.5.e588.

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The present study provides several lines of evidence which indicate that in the rat thymocyte adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5-cyclic monophosphate (cGMP) induce opposing regulatory effects on 2-deoxyglucose (2-DG) uptake; cAMP is stimulatory, whereas cGMP is inhibitory. First, the cyclic nucleotide analogues dibutyryl cAMP (dBcAMP) and dibutyryl cGMP (dBcGMP) produced a dose-related increase and decrease in thymocyte 2-DG uptake, respectively. Second, 3,5,3'-triiodo-L-thyronine (T3) and epinephrine, which increased cellular cAMP concentration but had no effect on
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Stricker, Stephen A. "Inhibition of germinal vesicle breakdown by antioxidants and the roles of signaling pathways related to nitric oxide and cGMP during meiotic resumption in oocytes of a marine worm." REPRODUCTION 143, no. 3 (2012): 261–70. http://dx.doi.org/10.1530/rep-11-0358.

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In mammalian oocytes, cAMP elevations prevent the resumption of meiotic maturation and thereby block nuclear disassembly (germinal vesicle breakdown (GVBD)), whereas nitric oxide (NO) and its downstream mediator cGMP can either inhibit or induce GVBD. Alternatively, some invertebrate oocytes use cAMP to stimulate, rather than inhibit, GVBD, and in such cases, the effects of NO/cGMP signaling on GVBD remain unknown. Moreover, potential interactions between NO/cGMP and AMP-activated kinase (AMPK) have not been assessed during GVBD. Thus, this study analyzed intraoocytic signaling pathways relate
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Dissertations / Theses on the topic "CAMP/cGMP"

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Schobesberger, Sophie. "Changes in cardiomyocyte structure and cAMP/cGMP signalling during heart failure." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/34341.

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The contractile function of the heart depends on efficient β adrenergic receptor (βAR) signalling which involves cycling nucleotides as second messengers. Correct secondary messenger signalling is only possible in healthy, well structured cardiac myocytes. Of the three βAR subtypes present in human cardiomyocytes β1AR and β2AR classically signal via 3'-5' cyclic adenosine monophosphate (cAMP) to regulate contraction after catecholamine administration, whereby the second isoform may also be cardioprotective. The far less characterised β3AR has been controversially associated to both increasing
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Assender, Jean W. "Control of vascular smooth muscle cell proliferation by cyclic nucleotides." Thesis, Cardiff University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389966.

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Janßen, Julia Annika. "In vivo FLIM-FRET as a novel technique to assess cAMP and cGMP in the intact zebrafish heart." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-232452.

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Introduction: 23 million patients worldwide suffer from heart failure. These patients depend on cardiac research, because cardiac research enables the development of new therapeutic strategies and –targets. In cardiomyocytes, the compartmentalization of cAMP and cGMP depends on many factors. T-tubuli and PDEs are responsible for the division of cells in microdomains in which localized and specific cAMP and cGMP-signaling occurs. The aim of this thesis was to develop a method to answer the open questions that remain about the physiological and pathophysiological significance of cAMP/cGMP compar
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Kühn, Rainer. "Untersuchungen zur Bedeutung der cAMP- und cGMP- abhängigen Signaltransduktion in der Kontrolle der glatten Muskulatur des humanen Ureters." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-84072.

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Karlisch, Kaja [Verfasser], and Andreas [Gutachter] Friebe. "Die Rolle der PDE3 im cGMP/cAMP-Crosstalk in NO-GC-defizienten Mäusen / Kaja Karlisch. Gutachter: Andreas Friebe." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1102826138/34.

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Kühn, Rainer. "Untersuchungen zur Bedeutung der cAMP- und cGMP- abhängigen Signaltransduktion in der Kontrolle der glatten Muskulatur des humanen Ureters : Eine funktionelle Studie." kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/8407/.

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Dünnes, Sarah [Verfasser], Andreas [Gutachter] Friebe, and Erhard [Gutachter] Wischmeyer. "Einfluss der NO-sensitiven Guanylyl-Cyclase auf den cGMP/cAMP-Crosstalk und die Steifigkeit der murinen Aorta / Sarah Dünnes ; Gutachter: Andreas Friebe, Erhard Wischmeyer." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1121508316/34.

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Marais, Erna. "Role of cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP) and p38 mitogen activated protein kinase (p38 MAPK) in preconditioning of the ischaemic myocardium." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/53039.

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Thesis (PhD)--University of Stellenbosch, 2002.<br>ENGLISH ABSTRACT: Ischaemic preconditioning (PC) is the phenomenon whereby a short episode of coronary occlusion followed by reperfusion protects the myocardium against a subsequent period of prolonged (also called index or sustained) ischaemia. Even though the exact mechanism of PC remains to be established, it implies that the heart has an endogenous protective mechanism against ischaemia which, if identified, may have important clinical implications. The importance of establishing the mechanism of PC lies in the potential to convert
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Dünnes, Sarah Verfasser], Andreas [Gutachter] [Friebe, and Erhard [Gutachter] Wischmeyer. "Einfluss der NO-sensitiven Guanylyl-Cyclase auf den cGMP/cAMP-Crosstalk und die Steifigkeit der murinen Aorta / Sarah Dünnes ; Gutachter: Andreas Friebe, Erhard Wischmeyer." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1121508316/34.

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MARTINS, Daniella Ramos. "Avaliação do relaxamento vascular induzido por um novo derivado pirazólico protótipo a fármaco (LQFM 021), possível inibidor de fosfodiesterase." Universidade Federal de Goiás, 2012. http://repositorio.bc.ufg.br/tede/handle/tde/2110.

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Made available in DSpace on 2014-07-29T16:11:50Z (GMT). No. of bitstreams: 1 Dissertacao DAniella Ramos Martins.pdf: 914272 bytes, checksum: 038f97a7fcd95721aab346f4a3bd0587 (MD5) Previous issue date: 2012-02-28<br>The inhibition of phosphodiesterases (PDEs) increases intracellular levels of cyclic nucleotides 3 ': 5'-cyclic adenosine monophosphate (cAMP) and 3 ': 5'-cyclic guanosine monophosphate (cGMP), which has many physiological and biochemical effects, especially in cardiovascular system. The objective of this study was to analyze the pharmacological effects of a new compound derived f
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Books on the topic "CAMP/cGMP"

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Schmidt, Ulrike. Secondary Messenger Systems in PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0014.

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Second messengers such as cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), inositoltriphosphate, and diacylglycerol (DAG) are a prerequisite for the signal transduction of extracellular receptors. The latter are central for cellular function and thus are implicated in the pathobiology of a variety of disorders, such as schizophrenia, bipolar disorder, major depression, and post-traumatic stress disorder (PTSD). This chapter focuses on the involvement of second messenger molecules and their regulators as direct targets in human and animal PTSD and aims to stimulate
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Book chapters on the topic "CAMP/cGMP"

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Corbin, Jackie D., Stephen J. Beebe, Charles E. Cobb, et al. "Signal Transduction through cAMP and cGMP." In Signal Transduction and Protein Phosphorylation. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-0166-1_2.

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Reverte-Salisa, Laia, Abhishek Sanyal, and Alexander Pfeifer. "Role of cAMP and cGMP Signaling in Brown Fat." In Brown Adipose Tissue. Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_117.

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Gjuric, M., N. Thürauf, and H. Hatt. "Charakterisierung und Differenzierung cAMP/cGMP-abhängiger Ionenkanäle olfaktorischer Sinnes- und Stützzellen." In Sitzungsbericht. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85188-9_58.

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Rascon, A., P. Belfrage, E. Degerman, et al. "Purification of a cGMP-inhibited cAMP Phosphodiesterase from Vascular Smooth Muscle." In Purines in Cellular Signaling. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_51.

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Taban, C. H., and M. Cathieni. "Second Messengers in Newt Limb Regeneration: cAMP and cGMP Levels and Distribution." In Recent Trends in Regeneration Research. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-9057-2_9.

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Lorenz, Robin, Daniela Bertinetti, and Friedrich W. Herberg. "cAMP-Dependent Protein Kinase and cGMP-Dependent Protein Kinase as Cyclic Nucleotide Effectors." In Non-canonical Cyclic Nucleotides. Springer International Publishing, 2015. http://dx.doi.org/10.1007/164_2015_36.

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Sassi, Yassine, and Jean-Sébastien Hulot. "Pulmonary Hypertension: Novel Pathways and Emerging Therapies Inhibitors of cGMP and cAMP Metabolism." In Handbook of Experimental Pharmacology. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-662-45805-1_20.

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Paul, N. E., K. Hemmrich, C. Gummersbach, C. V. Suschek, K. Kröncke, and N. Pallua. "The impact of cGMP and cAMP dependent pathways on the differentiation of human preadipocytes." In Deutsche Gesellschaft für Chirurgie. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_96.

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Whalin, M. W., S. J. Strada, J. G. Scammell, and W. J. Thompson. "Regulation of cAMP Metabolism in PC12 Cells by Type II (cGMP-Activatable) Cyclic Nucleotide Phosphodiesterase." In Purines in Cellular Signaling. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_47.

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Tegge, W., W. Dostmann, F. Hofmann, and R. Frank. "Determination of the specificities of cAMP— and cGMP— dependent protein kinases with peptide libraries on cellulose paper." In Peptides 1994. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_217.

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Conference papers on the topic "CAMP/cGMP"

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Maurice, D. H., and R. J. Haslam. "ROLES OF cAMP AND cGMP IN THE SYNERGISTIC INHIBITORY EFFECTS OF NITROVASODILATORS AND PGE1 ON PLATELET AGGREGATION AND DEGRANULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644533.

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Washed rabbit platelets labelled with [14C]5-HT and suspended in a modified Tyrode’s solution were used in this study. Incubation of the platelets with 0.1, 1 and 10 μM sodium nitro-prusside (SNP) for 30 s inhibited aggregation induced by 10 nM platelet-activating factor by 7, 13 and 45% and the release of [14C]5-HT by 16, 30 and 45%, respectively. In combination with 0.02 μM PGE1, which had little effect alone (7% inhibitions), these concentrations of SNP caused 58, 90 and 100% inhibitions of aggregation and 60, 73 and 81% inhibitions of [14C]5-HT release. Thus, SNP and PGE1 acted synergisti-
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Grant, P. G., A. F. Mannarino, and R. W. Colman. "REGULATION OF CYCLIC NUCLEOTIDE PHOSPHODIESTERASE ACTIVITY IN PLATELETS BY PHOSPHORYLATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642820.

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Cyclic nucleotide phosphodiesterases (PDE) provide the only known pathway for the hydrolysis of cyclic nucleotides in cells and thus have the potential for modulating the effects of cAMP and cGMP on cells. In platelets a rise in intracellular cAMP levels inhibits platelet aggregation and secretion. Since cAMP exerts many of its effects through a cAMP-dependent kinase we questioned whether phosphorylation of cAMP PDE might be a mode for regulation of PDE activity in platelets. When platelets were incubated for 10 min with forskolin (100 μM) the level of cAMP rose at least 10-fold.When the low K
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Khatib, SY, and A. Badwan. "Bronchodilation Effects of PDE5 Inhibitors (Sildenafil & Ordonofil): Role of cGMP/cAMP-NO." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2437.

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Ochoa, Cristhiaan, Mikhail Alexeyev, Dara Frank, and Troy Stevens. "Pseudomonas Aeruginosa Exotoxin Y Increases Intracellular Levels Of Both CAMP And CGMP In Pulmonary Microvascular Endothelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4179.

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Drndarski, Svetlana, Greg A. Knock, Philip I. Aaronson, and Jeremy P. T. Ward. "Diverging Effects Of The Cyclic Nucleotide Antagonists Rp-8Br-cGMP And Rp-8Br-cAMP In Rat Pulmonary And Mesenteric Artery." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6279.

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Asaji, T., E. Murakami, N. Takekoshi, S. Matsui, and T. Imaoka. "EFFECT OF ATRIAL NATRIURETIC POLYPEPTIDES ON PLATELET FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644872.

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Atrial natriuretic polypeptides (ANP) have been shown to possess a potent diuretic and natriuretic activity, and medicated to patients with heart insufficiency as a drug to be mediated by cGMPaccumulation in glomeruli. A existence of receptors for ANP have recently beenreported in human platelet. But, whether ANP has a direct effect on platelet function remains to be known.Single stimulation of ANP in any concentration did not induce aggregation in neither platelet rich plasma, nor washed platelets. Also no effect of pretreatment with ANP was observed against aggregation triggered by known med
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Moffat, Katrina J., and D. Euan MacIntyre. "REGULATION OF RECEPTOR-OPERATED Ca2− CHANNEL OPENING IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644677.

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Agonist-induced elevation of the platelet intracellular free Ca2+ concentration ([Ca2−]i), as monitored using quin2, is not electrically mediated and is attenuated by removal of extracellular Ca2− and by lanthanides (e.g Gd3−).Collectively these data suggest that elevation of [Ca2−]i in platelets derives in part via influx of external Ca2−presumably through a receptor-operated Ca2− channel (ROC). Hal lam &amp; Rink (FEBS Lett. 186: 175: 1985) showed that Mn2−also enters platelets via these ROC. To investigate the possible regulatory mechanisms that govern ROC status, we utilized quin2-labelled
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