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Journal articles on the topic 'Cyclic guanosine 3',5'-monophosphate'

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Author: Grafiati

Published: 6 September 2023

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1

Srivastava, Uma S., Manohar Lal Thakur, and C. Spach. "Cyclic 3′, 5′-adenosine monophosphate and cyclic 3′, 5′-guanosine monophosphate metabolism in malnutrition." Nutrition Research 6, no. 5 (May 1986): 589–99. http://dx.doi.org/10.1016/s0271-5317(86)80113-0.

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2

Boadu, Emmanuel, Svanhild Vaskinn, Elisabeth Sundkvist, Ragnhild Jaeger, and Georg Sager. "Inhibition by guanosine cyclic monophosphate (cGMP) analogues of uptake of [3H]3′,5′-cGMP without stimulation of ATPase activity in human erythrocyte inside-out vesicles11Abbreviations: 3′,5′-cGMP, guanosine 3′,5′-cyclic monophosphate; 2′,3′-cGMP, guanosine 2′,3′-cyclic monophosphate; N-mb-cGMP, N2-monobutyryl guanosine 3′,5′-cyclic monophosphate; O-mb-cGMP, 2′-O-monobutyryl guanosine 3′,5′-cyclic monophosphate; Db-cGMP, N2,2′-O-dibutyryl guanosine 3′,5′-cyclic monophosphate; Br-cGMP, 8′-bromo guanosine 3′,5′-cyclic monophosphate; Rp-cGMPS, Rp-monophosphorothioate guanosine 3′,5′-cyclic monophosphate; Sp-cGMPS, Sp-monophosphorothioate guanosine 3′,5′-cyclic monophosphate; 3′,5′-cAMP, Adenosine 3′,5′-cyclic monophosphate; and MRP, multidrug resistance protein." Biochemical Pharmacology 62, no. 4 (August 2001): 425–29. http://dx.doi.org/10.1016/s0006-2952(01)00682-7.

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3

Pradelles, Philippe, Jacques Grassi, Danielle Chabardes, and Nicole Guiso. "Enzyme immunoassays of adenosine cyclic 3',5'-monophosphate and guanosine cyclic 3',5'-monophosphate using acetylcholinesterase." Analytical Chemistry 61, no. 5 (March 1989): 447–53. http://dx.doi.org/10.1021/ac00180a014.

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4

Beste, Kerstin Y., and Roland Seifert. "cCMP, cUMP, cTMP, cIMP and cXMP as possible second messengers: Development of a hypothesis based on studies with soluble guanylyl cyclase α1β1." Biological Chemistry 394, no. 2 (February 1, 2013): 261–70. http://dx.doi.org/10.1515/hsz-2012-0282.

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Abstract Adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate are second messengers that regulate multiple physiological functions. The existence of additional cyclic nucleotides in mammalian cells was postulated many years ago, but technical problems hampered development of the field. Using highly specific and sensitive mass spectrometry methods, soluble guanylyl cyclase has recently been shown to catalyze the formation of several cyclic nucleotides in vitro. This minireview discusses the broad substrate-specificity of soluble guanylyl cyclase and the possible second messenger roles of cyclic nucleotides other than adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate. We hope that this article stimulates productive and critical research in an area that has been neglected for many years.

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5

Meskini, N., O. MacOvschi, A. F. Prigent, G. Nemoz, P. Chapuy, and M. Lagarde. "Decreased Cyclic Nucleotide Phosphodiesterase Activity in Human Peripheral Blood Mononuclear Cells from Elderly Women." Clinical Science 79, no. 5 (November 1, 1990): 467–70. http://dx.doi.org/10.1042/cs0790467.

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1. Both adenosine 3′:5′-cyclic monophosphate and guanosine 3′:5′-cyclic monophosphate phosphodiesterase activities of peripheral blood mononuclear cells were markedly decreased in elderly women as compared with young control women. 2. In contrast, the ability of these cells to bind guanosine 5′-[β, γ-imido]triphosphate, a non-hydrolysable analogue of guanosine 5′-triphosphate, was the same in both groups. 3. These findings are discussed in the context of the decline in immune function which occurs with increasing age.

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6

Mattana, J., and P. C. Singhal. "Effects of atrial natriuretic peptide and cGMP on uptake of IgG complexes by macrophages." American Journal of Physiology-Cell Physiology 265, no. 1 (July 1, 1993): C92—C98. http://dx.doi.org/10.1152/ajpcell.1993.265.1.c92.

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Macromolecular handling by macrophages and glomerular mesangial cells may be important in the development of renal injury. We undertook the present study to determine whether atrial natriuretic peptide (ANP), a particulate guanylate cyclase stimulator, plays a direct role in uptake of immunoglobulin G (IgG) complexes by macrophages. Macrophages incubated with ANP at 10(-5) and 10(-6) M showed significantly suppressed uptake of IgG complexes compared with control. Macrophage uptake of IgG complexes was also significantly suppressed by the soluble guanylate cyclase stimulator sodium nitroprusside. Dibutyryl guanosine 3',5'-cyclic monophosphate and dibutyryl adenosine 3',5'-cyclic monophosphate both significantly suppressed IgG complex uptake as well. ANP was found to significantly enhance macrophage guanosine 3',5'-cyclic monophosphate (cGMP) levels compared with control cells, and this effect was antagonized by angiotensin II. Angiotensin II significantly enhanced uptake of IgG complexes and suppressed macrophage adenosine 3',5'-cyclic monophosphate synthesis, and both effects were antagonized by coincubation with ANP. These results suggest that ANP modulates uptake of IgG complexes by macrophages and that this effect may be mediated via cGMP.

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7

Géigel, LF, and LL Leon. "Cyclic 3'-5' guanosine monophosphate-dependent activity in Leishmania amazonensis." Memórias do Instituto Oswaldo Cruz 98, no. 4 (June 2003): 499–500. http://dx.doi.org/10.1590/s0074-02762003000400012.

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8

Santy, L. C., and G. Guidotti. "Reconstitution and characterization of two forms of cyclic nucleotide-gated channels from skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 271, no. 6 (December 1, 1996): E1051—E1060. http://dx.doi.org/10.1152/ajpendo.1996.271.6.e1051.

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A cyclic nucleotide-gated channel present in skeletal muscle plasma membrane has previously been identified as being responsible for insulin-activated sodium entry into muscle cells (J. E. M. McGeoch and G. Guidotti. J. Biol. Chem. 267:832-841, 1992). We have isolated this channel activity to further study and characterize it. The channel was solubilized from rabbit skeletal muscle sarcolemma and functionally reconstituted into phospholipid vesicles, as assayed by patch-clamp analysis of the reconstituted proteins. Channel activity was isolated by 8-bromo-guanosine 3',5'-cyclic monophosphate affinity chromatography, producing two distinct peaks of cyclic nucleotide-gated channel activity. These two types of channel activity differ in guanosine 3',5'-cyclic monophosphate affinity and in the ability to be opened by adenosine 3',5'-cyclic monophosphate. The cyclic nucleotide-gated channel from rod outer segments also forms two peaks of activity when purified in this manner. The presence of two forms of channel activity could have implications for the mechanism of insulin-activated sodium entry.

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9

Chen, Da-Chung, Shyng-Shiou F. Yuan, Her-Young Su, Shin-Chieh Lo, Shin-Sia Ren, and Gwo-Jang Wu. "Urinary cyclic guanosine 3′,5′-monophosphate and cyclic adenosine 3′,5′-monophosphate changes in spontaneous and induced onset active labor." Acta Obstetricia et Gynecologica Scandinavica 84, no. 11 (October 17, 2005): 1081–86. http://dx.doi.org/10.1111/j.0001-6349.2005.00831.x.

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10

Horton, J. K., R. C. Martin, S. Kalinka, A. Cushing, J. P. Kitcher, M. J. O'Sullivan, and P. M. Baxendale. "Enzyme immunoassays for the estimation of adenosine 3',5'cyclic monophosphate and guanosine 3',5'cyclic monophosphate in biological fluids." Journal of Pharmacological and Toxicological Methods 29, no. 4 (August 1993): 234. http://dx.doi.org/10.1016/1056-8719(93)90032-a.

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11

Horton, J. K., R. C. Martin, S. Kalinka, A. Cushing, J. P. Kitcher, M. J. O'Sullivan, and P. M. Baxendale. "Enzyme immunoassays for the estimation of adenosine 3′,5′ cyclic monophosphate and guanosine 3′,5′ cyclic monophosphate in biological fluids." Journal of Immunological Methods 155, no. 1 (October 1992): 31–40. http://dx.doi.org/10.1016/0022-1759(92)90268-x.

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12

Seymour, Andrea A., Benoni Abboa-Offei, Magdi M. Asaad, and W. Lynn Rogers. "Evaluation of SQ 28 603, an inhibitor of neutral endopeptidase, in conscious monkeys." Canadian Journal of Physiology and Pharmacology 69, no. 10 (October 1, 1991): 1609–17. http://dx.doi.org/10.1139/y91-238.

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The potent neutral endopeptidase inhibitor SQ 28 603 (N-(2-(mercaptomethyl)-1-oxo-3-phenylpropyl)-β-alanine) significantly increased excretion of sodium from 4.9 ± 2.3 to 14.3 ± 2.1 μequiv./min and cyclic 3′,5′-guanosine monophosphate from 118 ± 13 to 179 ± 18 pmol/min after intravenous administration of 300 μmol/kg (~80 mg/kg) in conscious female cynomolgus monkeys. SQ 28 603 did not change blood pressure or plasma atrial natriuretic peptide concentrations in the normal monkeys. In contrast, 1-h infusions of 3, 10, or 30 pmol∙kg−1∙min−1 of human atrial natriuretic peptide lowered blood pressure by −3 ± 4, −9 ± 4, and −27 ± 3 mmHg (1 mmHg = 133.322 Pa), increased cyclic guanosine monophosphate excretion from 78 ± 11 to 90 ± 6, 216 ± 33, and 531 ± 41 pmol/min, and raised plasma atrial natriuretic peptide from 7.2 ± 0.7 to 21 ± 4, 62 ± 12, and 192 ± 35 fmol/mL without affecting sodium excretion. In monkeys receiving 10 pmol∙kg−1∙min−1 of atrial natriuretic peptide, 300 μmol/kg of SQ 28 603 reduced mean arterial pressure by −13 ± 5 mmHg and increased sodium excretion from 6.6 ± 3.2 to 31.3 ± 6.0 μequiv./min, cyclic guanosine monophosphate excretion from 342 ± 68 to 1144 ± 418 pmol/min, and plasma atrial natriuretic peptide from 124 ± 8 to 262 ± 52 fmol/mL. In conclusion, SQ 28 603 stimulated renal excretory function in conscious monkeys, presumably by preventing the degradation of atrial natriuretic peptide by neutral endopeptidase.Key words: atrial natriuretic peptide, neutral endopeptidase, natriuresis, cyclic guanosine monophosphate.

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13

Lauria, Michele R., Cynthia A. Standley, Yoram Sorokin, Jill C. Todt, Sidney F. Bottoms, Frank D. Yelian, and David B. Cotton. "Brain Natriuretic Peptide and Cyclic Guanosine-3′,5′ Monophosphate in Preeclampsia." Journal of Maternal-Fetal and Neonatal Medicine 5, no. 3 (January 1996): 128–31. http://dx.doi.org/10.3109/14767059609025412.

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14

Son, Jong-Keun, and John P. N. Rosazza. "Cyclic Guanosine-3′,5′-Monophosphate and Biopteridine Biosynthesis in Nocardia sp." Journal of Bacteriology 182, no. 13 (July 1, 2000): 3644–48. http://dx.doi.org/10.1128/jb.182.13.3644-3648.2000.

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ABSTRACT Nocardia sp. strain NRRL 5646 contains a nitric oxide synthase (NOS) enzyme system capable of generating nitric oxide (NO) from arginine and arginine-containing peptides. To explain possible roles of the NOS system in this bacterium, guanylate cyclase (GC) and tetrahydrobiopterin (H4B) biosynthetic enzymes were identified in cell extracts and in culture media. Cell extracts contained GC activity, as measured by the conversion of GTP to cyclic guanosine-3′,5′-monophosphate (cGMP) at 9.56 pmol of cGMP h−1 mg of protein−1. Concentrations of extracellular cGMP in culture media were significantly increased, from average control levels of 45 pmol cGMP liter−1 to a maximum of 315 pmol liter−1, in response to additions of GTP, l-arginine, H4B, and sodium nitroprusside to growing Nocardia cultures. On the other hand, the NOS inhibitor N G-nitro-l-arginine and the GC inhibitor 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one both dramatically decreased extracellular cGMP levels. Activities for GTP-cyclohydrase-1,6-pyruvoyltetrahydropterin synthase and sepiapterin reductase, enzymes essential for H4B biosynthesis, were present in Nocardia culture extracts at 77.5 pmol of neopterin and 45.8 pmol of biopterin h−1 mg of protein−1, respectively. In Nocardia spp., as in mammals, GTP is a key intermediate in H4B biosynthesis, and GTP is converted to cGMP by a GC enzyme system that is activated by NO.

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15

Siragy, H. M., R. A. Johns, M. J. Peach, and R. M. Carey. "Nitric oxide alters renal function and guanosine 3',5'-cyclic monophosphate." Hypertension 19, no. 6_pt_2 (June 1992): 775–79. http://dx.doi.org/10.1161/01.hyp.19.6.775.

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16

Navarro, José Antonio, Félix Javier Jiménez-Jiménez, José Antonio Molina, Julián Benito-León, Elena Cisneros, Teresa Gasalla, Miguel Ortı́-Pareja, Antonio Tallón-Barranco, Fernando de Bustos, and Joaquı́n Arenas. "Cerebrospinal fluid cyclic guanosine 3′5′ monophosphate levels in Parkinson's disease." Journal of the Neurological Sciences 155, no. 1 (February 1998): 92–94. http://dx.doi.org/10.1016/s0022-510x(97)00267-0.

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17

Teran, Enrique, Carlos Escudero, Sandra Vivero, Armando Enriquez, and Andres Calle. "Intraplatelet Cyclic Guanosine‐3′,5′‐Monophosphate Levels During Pregnancy and Preeclampsia." Hypertension in Pregnancy 23, no. 3 (January 2004): 303–8. http://dx.doi.org/10.1081/prg-200030860.

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18

Wu, Chung-Pu, Hannah Woodcock, Stephen B. Hladky, and Margery A. Barrand. "cGMP (guanosine 3′,5′-cyclic monophosphate) transport across human erythrocyte membranes." Biochemical Pharmacology 69, no. 8 (April 2005): 1257–62. http://dx.doi.org/10.1016/j.bcp.2005.02.005.

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19

Stroiński, A., and J. Floryszak-Wieczorek. "Guanosine 3′:5′-cyclic monophosphate changes during germination of Hordeum vulgare." Plant Science 42, no. 1 (December 1985): 1–4. http://dx.doi.org/10.1016/0168-9452(85)90020-2.

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20

Benson, Jeffrey Alan. "The effects of cyclic 3′5′ adenosine monophosphate and cyclic 3′5′ guanosine monophosphate upon sutural expansion by an orthopedic force." American Journal of Orthodontics 88, no. 2 (August 1985): 175. http://dx.doi.org/10.1016/0002-9416(85)90248-9.

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21

Henrich, W. L., E. A. McAllister, P. B. Smith, and W. B. Campbell. "Guanosine 3',5'-cyclic monophosphate as a mediator of inhibition of renin release." American Journal of Physiology-Renal Physiology 255, no. 3 (September 1, 1988): F474—F478. http://dx.doi.org/10.1152/ajprenal.1988.255.3.f474.

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The role of guanosine 3',5'-cyclic monophosphate (cGMP) as an inhibitory mediator of tissue renin release was examined in two different in vitro preparations. In rat superficial cortical slices, renin release stimulated by isoproterenol (10(-5) M) was ablated by atriopeptin III (ANP, 2.1 x 10(-8) M), nitroprusside (NP, 10(-3) M), and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 10(-3) and 10(-6) M). Arachidonic acid (10(-3) M)-stimulated renin release was also inhibited by ANP and 8-BrcGMP (10(-3) and 10(-6) M). Both ANP and NP increased tissue cGMP concentrations significantly (P less than 0.05), but neither had an effect on adenosine 3',5'-cyclic monophosphate (cAMP) concentrations. When methylene blue (10(-5) M), an inhibitor of guanylate cyclase, was added to slices incubated with isoproterenol and ANP, the inhibition of renin release by ANP was abolished. These results were confirmed in a preparation of isolated cultured rat juxtaglomerular cells. In these cells, isoproterenol induced a significant increase (58%, P less than 0.01) in renin release, which was inhibited by the addition of 8-BrcGMP (10(-6) M). These data demonstrate a direct inhibitory effect of ANP on isoproterenol- and arachidonic acid-induced renin release. The results with NP, 8-BrcGMP, and methylene blue suggest that cGMP is an intracellular mediator of this inhibition.

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22

Lee, S. L., W. W. Wang, and B. L. Fanburg. "Nitroprusside inhibits serotonin-induced mitogenesis and tyrosine phosphorylation of smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (March 1, 1996): L362—L367. http://dx.doi.org/10.1152/ajplung.1996.270.3.l362.

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Serotonin (5-hydroxytryptamine, 5-HT) produces hyperplasia and hypertrophy of bovine pulmonary artery smooth muscle cells (SMC) in culture. The growth responses are associated with early elevations of c-myc and actin gene expressions and are blocked by agents that elevate cellular adenosine 3',5'-cyclic monophosphate or inhibit 5-HT transport or tyrosine phosphorylation. A rapid enhancement of tyrosine phosphorylation of a 120-kDa protein (p120) is associated with the 5-HT-induced mitogenesis. In the present studies, sodium nitroprusside (SNP, 10-100 micromol/l), a NO-generating agent, dose dependently inhibited 5-HT-induced thymidine incorporation by SMC. Inhibition of the 5-HT stimulatory effect was also observed with isosorbide dinitrate and nitroglutathione, which are also NO donors. Incubation of cells with 8-bromoguanosine 3',5'-cyclic monophosphate (1 micromol/l) mimicked the antimitogenic action of SNP. The antiproliferative effect of SNP was inhibited by hemoglobin (50 micromol/l) and potentiated by superoxide dismutase (200 U/ml), supporting the role of NO in the process. Enhancement of tyrosine phosphorylation of p120 by 5-HT was prevented by preincubation with SNP or exogenously added guanosine 3',5'-cyclic monophosphate. The data indicate that 5-HT acts as a mitogen for SMC through a signal transduction pathway involving tyrosine phosphorylation. SNP likely prevents the 5-HT-induced mitogenesis of SMC through elevation of intracellular guanosine 3',5'-cyclic monophosphate and inhibition of tyrosine phosphorylation of p120.

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23

Titus, Steven A., Xiao Li, Noel Southall, Jianming Lu, James Inglese, Michael Brasch, Christopher P. Austin, and Wei Zheng. "A Cell-Based PDE4 Assay in 1536-Well Plate Format for High-Throughput Screening." Journal of Biomolecular Screening 13, no. 7 (July 1, 2008): 609–18. http://dx.doi.org/10.1177/1087057108319977.

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The cyclic nucleotide phosphodiesterases (PDEs) are intracellular enzymes that catalyze the hydrolysis of 3,′5′-cyclic nucleotides, such as cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), to their corresponding 5′nucleotide monophosphates. These enzymes play an important role in controlling cellular concentrations of cyclic nucleotides and thus regulate a variety of cellular signaling events. PDEs are emerging as drug targets for several diseases, including asthma, cardiovascular disease, attention-deficit hyperactivity disorder, Parkinson's disease, and Alzheimer's disease. Although biochemical assays with purified recombinant PDE enzymes and cAMP or cGMP substrate are commonly used for compound screening, cell-based assays would provide a better assessment of compound activity in a more physiological context. The authors report the development and validation of a new cell-based PDE4 assay using a constitutively active G-protein—coupled receptor as a driving force for cAMP production and a cyclic nucleotide—gated cation channel as a biosensor in 1536-well plates. ( Journal of Biomolecular Screening 2008:609-618)

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24

Prakash, Y. S., Adeyemi Iyanoye, Binnaz Ay, Gary C. Sieck, and Christina M. Pabelick. "Store-operated Ca2+Influx in Airway Smooth Muscle." Anesthesiology 105, no. 5 (November 1, 2006): 976–83. http://dx.doi.org/10.1097/00000542-200611000-00019.

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Background Volatile anesthetics produce bronchodilation in part by depleting sarcoplasmic reticulum Ca stores in airway smooth muscle (ASM). Other bronchodilatory drugs are known to act via cyclic nucleotides (cyclic adenosine 3',5'-cyclic monophosphate, cyclic guanosine 3',5'-cyclic monophosphate). Intracellular Ca regulation in ASM involves plasma membrane Ca influx, including that triggered by sarcoplasmic reticulum Ca depletion (store-operated Ca entry [SOCE]). The authors hypothesized that anesthetics and bronchodilatory agents interact in inhibiting SOCE, thus enhancing ASM relaxation. Methods In enzymatically dissociated porcine ASM cells imaged using fluorescence microscopy, sarcoplasmic reticulum Ca was depleted by 1 microm cyclopiazonic acid in 0 extracellular Ca, nifedipine, and potassium chloride (preventing Ca influx through L-type channels and SOCE). Extracellular Ca was rapidly reintroduced to selectively activate SOCE in the presence or absence of 1 minimum alveolar concentration (MAC) halothane, isoflurane, or sevoflurane. Anesthetic interference with SOCE regulation by cyclic nucleotides was examined by activating SOCE in the presence of (1) 1 microm acetylcholine, (2) 100 microm dibutryl cyclic adenosine 3',5'-cyclic monophosphate, or (3) 100 microm 8-bromo-cyclic guanosine 3',5'-cyclic monophosphate. Results SOCE was enhanced by acetylcholine, whereas volatile anesthetics and both cyclic nucleotides partially inhibited Ca influx. Preexposure to 1 or 2 MAC anesthetic (halothane > isoflurane > sevoflurane) inhibited SOCE. Only halothane and isoflurane inhibited acetylcholine-induced augmentation of Ca influx, and significantly potentiated cyclic nucleotide inhibition such that no influx was observed in the presence of anesthetics and cyclic nucleotides. Conclusions These data indicate that volatile anesthetics prevent sarcoplasmic reticulum refilling by inhibiting SOCE and enhancing cyclic nucleotide blunting of Ca influx in ASM. Such interactions likely result in substantial airway relaxation in the presence of both anesthetics and bronchodilatory agents such as beta agonists or nitric oxide.

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25

Kamynina, Alisa, Sebastian Guttzeit, Philip Eaton, and Friederike Cuello. "Nitroxyl Donor CXL-1020 Lowers Blood Pressure by Targeting C195 in Cyclic Guanosine-3’,5’-Monophosphate-Dependent Protein Kinase I." Hypertension 79, no. 5 (May 2022): 946–56. http://dx.doi.org/10.1161/hypertensionaha.122.18756.

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Background: We previously demonstrated that nitroxyl causes vasodilation, at least in part, by inducing the formation of an intradisulfide bond between C117 and C195 in the high affinity cyclic guanosine monophosphate-binding site of PKGI (cyclic guanosine monophosphate-dependent protein kinase I). The aim of this study was to determine whether nitroxyl donors lower blood pressure via this novel PKGI activation mechanism in vivo. Methods: To determine this, a C195S PKGI knock-in mouse model was generated that ubiquitously and constitutively expresses a mutant kinase resistant to nitroxyl-induced intradisulfide activation. Results: Knock-in and wild-type littermates did not differ in appearance, body weight, in PKGI protein expression or blood gas content. Organ weight was similar between genotypes apart from the cecum that was significantly enlarged in knock-in animals. Mean arterial pressure and heart rate monitored in vivo over 24 hours by radio-telemetry revealed neither a significant difference between genotypes at baseline nor during angiotensin II–induced hypertension or sepsis. CXL-1020, a clinically relevant nitroxyl donor, did not lower blood pressure in normotensive animals. In contrast, administering CXL-1020 to hypertensive wild-type mice reduced their blood pressure by 10±4 mm Hg ( P =0.0184), whereas the knock-in littermates were unaffected. Conclusions: Oxidation of C195 in PKGI contributes to the antihypertensive effects observed in response to nitroxyl donors, emphasising the potential importance of nitroxyl donors in pathological scenarios when cyclic guanosine monophosphate levels are reduced and insufficient to activate PKGI.

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26

Bkaily, G., and N. Sperelakis. "Injection of guanosine 5'-cyclic monophosphate into heart cells blocks calcium slow channels." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 5 (May 1, 1985): H745—H749. http://dx.doi.org/10.1152/ajpheart.1985.248.5.h745.

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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.

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27

Range, Simon P., Elaine D. Holland, Graham P. Basten, and Alan J. Knox. "Regulation of guanosine 3′:5′-cyclic monophosphate in ovine tracheal epithelial cells." British Journal of Pharmacology 120, no. 7 (March 1997): 1249–54. http://dx.doi.org/10.1038/sj.bjp.0701040.

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28

Burke-Wolin, T., C. J. Abate, M. S. Wolin, and G. H. Gurtner. "Hydrogen peroxide-induced pulmonary vasodilation: role of guanosine 3',5'-cyclic monophosphate." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 6 (December 1, 1991): L393—L398. http://dx.doi.org/10.1152/ajplung.1991.261.6.l393.

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Hydrogen peroxide (H2O2), but not tertbutyl hydroperoxide, produces a concentration-dependent vasodilation of the pulmonary circulation in isolated saline perfused rabbit lungs when pulmonary arterial pressures (PAP) are raised with the thromboxane analogue U-46619. This vasodilation was enhanced in the presence of indomethacin, suggesting that H2O2 possesses both a prostaglandin-mediated constrictor and an additional dilator mechanism. In isolated rabbit intrapulmonary arteries the endothelium did not alter the dose-dependent relaxation of arterial rings to H2O2, and indomethacin enhanced the relaxant response of the peroxide. The decrease in PAP and relaxation of isolated pulmonary arteries observed with H2O2 was attenuated with 10 microM methylene blue, an inhibitor of soluble guanylate cyclase activation. M & B 22948, a guanosine 3',5'-cyclic monophosphate (cGMP)-selective phosphodiesterase inhibitor, enhanced the vasodilation or relaxation to the peroxide in both preparations. These changes were not endothelium dependent. Inhibition of the cGMP-associated endothelium-derived relaxant factor (EDRF) with nitro-L-arginine, did not alter relaxation of arterial rings to peroxide. Thus H2O2 appears to produce pulmonary vasodilation through the activation of guanylate cyclase and accumulation of cGMP. Both H2O2 and EDRF may function as tonic stimulators of guanylate cyclase in the pulmonary circulation and contribute to the maintenance of low basal pressures.

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29

Hegde, V. R., H. Wittreich, M. G. Patel, A. C. Horan, R. F. Hart, J. J. Troyanovich, M. S. Puar, and V. P. Gullo. "Naturally produced isocoumarins: inhibitors of calmodulinsensitive cyclic guanosine 3′,5′-monophosphate phosphodiesterase." Journal of Industrial Microbiology 4, no. 3 (May 1989): 209–13. http://dx.doi.org/10.1007/bf01574078.

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30

Cummings, James J., and Huamei Wang. "Nitric oxide decreases lung liquid production via guanosine 3′,5′-cyclic monophosphate." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 5 (May 1, 2001): L923—L929. http://dx.doi.org/10.1152/ajplung.2001.280.5.l923.

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We studied the role of cGMP in nitric oxide (NO)-induced changes in lung liquid production ( J v ) in chronically instrumented fetal sheep. Forty-five studies were done in which J v was measured by a tracer dilution technique. Left pulmonary arterial flow (Qlpa) was measured by a Doppler flow probe. There were two series of experiments. In the first, we gave 8-bromo-cGMP, a cGMP analog, by either the pulmonary vascular or intraluminal route; in the second, we used agents to inhibit or enhance endogenous cGMP activity. When infused directly into the pulmonary circulation, 8-bromo-cGMP significantly increased Qlpa but had no effect on J v. Conversely, when instilled into the lung liquid, 8-bromo-cGMP had no effect on Qlpa but significantly reduced J v. Inhibition of guanylate cyclase activity with methylene blue totally blocked, whereas phosphodiesterase inhibition with Zaprinast significantly enhanced, the effect of instilled NO on J v. Thus the reduction in lung liquid caused by NO appears to be mediated by cGMP, perhaps through a direct effect on the pulmonary epithelium.

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Sugawa, Makoto, Kazuhiko Tamura, Tohru Koide, and Shigetaka Naitoh. "Functional roles of cyclic guanosine 3′,5′-monophosphate analogue in cerebral vasodilation." General Pharmacology: The Vascular System 24, no. 3 (May 1993): 577–84. http://dx.doi.org/10.1016/0306-3623(93)90214-i.

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Lauria, Michele R., Cynthia A. Standley, Yoram Sorokin, Jill C. Todt, Sidney F. Bottoms, Frank D. Yellan, and David B. Cotton. "Brain natriuretic peptide and cyclic guanosine-3?,5? monophosphate in pre-eclampsia." Journal of Maternal-Fetal Medicine 5, no. 3 (May 1996): 128–31. http://dx.doi.org/10.1002/(sici)1520-6661(199605/06)5:3<128::aid-mfm6>3.0.co;2-o.

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33

Lee, HC. "A Signaling Pathway Involving Cyclic ADP-Ribose, cGMP, and Nitric Oxide." Physiology 9, no. 3 (June 1, 1994): 134–37. http://dx.doi.org/10.1152/physiologyonline.1994.9.3.134.

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Cyclic nucleotides are second messengers effecting changes mainly through protein phosphorylation. Cyclic ADP-ribose (cADPR), a newly discovered member, instead exerts its function through calcium mobilization. Increasing evidence suggests that cADPR may mediate the effects of nitric oxide on calcium, with guanosine 3', 5'-cyclic monophosphate serving as an intermediate.

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34

De Vente, J., H. W. M. Steinbusch, and J. Schipper. "A new approach to immunocytochemistry of 3′,5′-cyclic guanosine monophosphate: Preparation, specificity, and initial application of a new antiserum against formaldehyde-fixed 3′,5′-cyclic guanosine monophosphate." Neuroscience 22, no. 1 (July 1987): 361–73. http://dx.doi.org/10.1016/0306-4522(87)90226-0.

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35

Jarratt-Barnham, Edwin, Limin Wang, Youzheng Ning, and Julia M. Davies. "The Complex Story of Plant Cyclic Nucleotide-Gated Channels." International Journal of Molecular Sciences 22, no. 2 (January 16, 2021): 874. http://dx.doi.org/10.3390/ijms22020874.

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Plant cyclic nucleotide-gated channels (CNGCs) are tetrameric cation channels which may be activated by the cyclic nucleotides (cNMPs) adenosine 3′,5′-cyclic monophosphate (cAMP) and guanosine 3′,5′-cyclic monophosphate (cGMP). The genome of Arabidopsis thaliana encodes 20 CNGC subunits associated with aspects of development, stress response and immunity. Recently, it has been demonstrated that CNGC subunits form heterotetrameric complexes which behave differently from the homotetramers produced by their constituent subunits. These findings have widespread implications for future signalling research and may help explain how specificity can be achieved by CNGCs that are known to act in disparate pathways. Regulation of complex formation may involve cyclic nucleotide-gated channel-like proteins.

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Pinto, Emilia Modolo, Fabio R. Faucz, Luana Z. Paza, Gang Wu, Elizabeth S. Fernandes, Jerome Bertherat, Constantine A. Stratakis, et al. "Germline Variants in Phosphodiesterase Genes and Genetic Predisposition to Pediatric Adrenocortical Tumors." Cancers 12, no. 2 (February 22, 2020): 506. http://dx.doi.org/10.3390/cancers12020506.

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Phosphodiesterases (PDEs) form a superfamily of enzymes that catalyze the hydrolysis of cyclic nucleotides adenosine 3′5′-cyclic monophosphate (cAMP) and guanosine 3′5′-cyclic monophosphate (cGMP) to their inactive 5′ monophosphates. cAMP plays a critical role as a second messenger in endocrine tissues, and activation of cAMP signaling has been reported in endocrine tumors. Germline variants in PDEs have been associated with benign cortisol-secreting adrenocortical adenomas and testicular germ cell cancer but not adrenocortical carcinoma. We performed whole genome sequencing (WGS) and whole exome sequencing (WES) of paired blood and tumor samples from 37 pediatric adrenocortical tumors (ACTs). Germline inactivating variants in PDEs were observed in 9 of 37 (24%) patients. Tumor DNA analysis revealed loss of heterozygosity, with maintenance of the mutated allele in all cases. Our results suggest that germline variants in PDEs and other regulators of the cAMP-signaling pathway may contribute to pediatric adrenocortical tumorigenesis, perhaps by cooperating with germline hypomorphic mutant TP53 alleles and uniparental disomy of chromosome 11p15 (Beckwith–Wiedemann syndrome).

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McGrogan, I., S. Lu, S. Hipworth, L. Sormaz, R. Eng, D. Preocanin, and E. E. Daniel. "Mechanisms of cyclic nucleotide-induced relaxation in canine tracheal smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 3 (March 1, 1995): L407—L413. http://dx.doi.org/10.1152/ajplung.1995.268.3.l407.

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The effects of exogeneous cyclopiazonic acid (CPA, 10 microM), a selective inhibitor of the sarcoplasmic reticulum (SR) Ca2+ adenosinetriphosphatase, on cyclic nucleotide-induced relaxations of canine airway smooth muscle were examined. Strips of tracheal muscle were precontracted with carbachol (50% median effective concentration, 0.1 microM) or with 60 mM KCl. The beta-agonist isoproterenol (ISO, 10 microM) relaxed the tissue by approximately 50%. The relaxation was reduced in the presence of CPA when L-type Ca2+ channels were available but not when these were blocked by 0.1 microM nifedipine. Forskolin (1.0 microM), an adenylate cyclase activator, was less effective at inhibiting the contraction than ISO, and addition of CPA did not block its inhibitory effect as effectively as when ISO was used. Radioimmunoassay indicated that both these agents raised adenosine 3',5'-cyclic monophosphate (cAMP) levels to the same degree. Very little relaxation of the precontracted smooth muscle was elicited by 3 mM 8-bromo-adenosine 3',5'-cyclic monophosphate (8-BrcAMP), and addition of CPA had no effect. Sodium nitroprusside (100 microM) and 8-bromo-guanosine 3',5'-cyclic monophosphate (10 mM) inhibited contraction to a greater degree than any agent that raised cAMP. These inhibitions were greatly reduced in the presence of CPA when L-type Ca2+ channels were available. We conclude that pumping of Ca2+ into SR plays a major role guanosine 3',5'-cyclic monophosphate-produced but not cAMP-induced relaxation; L-type Ca2+ channels must be available for the relaxant role of Ca2+ pumping into the SR to be expressed; and ISO-induced relaxation may not involve primarily elevation of the cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Garty, H., O. Yeger, A. Yanovsky, and C. Asher. "Guanosine nucleotide-dependent activation of the amiloride-blockable Na+ channel." American Journal of Physiology-Renal Physiology 256, no. 5 (May 1, 1989): F965—F969. http://dx.doi.org/10.1152/ajprenal.1989.256.5.f965.

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Effects of guanosine nucleotides on the epithelial Na+ channel were studied in apical membrane vesicles derived from the toad bladder epithelium. Trapping 10 microM guanosine-5'-O-(thiotriphosphate) (GTP gamma S) in vesicles evoked two- to fourfold increase in the amiloride-sensitive (Na+ channel-mediated) 22Na+ uptake. The nucleotide had no significant effect on the amiloride-insensitive 22Na+ uptake or the valinomycin-mediated 86Rb+ uptake in the same membranes. The stimulatory action of GTP gamma S was mimicked by 5'-guanylylimidiodiphosphate (GppNHp) and could at least partly be reversed by guanosine-5'-O-(thiodiphosphate) (GDP beta S) (10-fold excess). GTP itself and adenosine-5'-O-(thiotriphosphate) (ATP gamma S) had no sustained effect on Na+ transport in vesicles. Thus it appears that the epithelial Na+ channel is directly or indirectly regulated by the occupancy of a guanosine-specific site, probably the alpha subunit of a G protein. The possibility that GTP gamma S acts indirectly by activating a membrane-bound, GTP-dependent enzyme the product of which modulates the channel conductance was assessed by measuring 22Na+ fluxes in membrane vesicles prepared to contain products of such enzymes. None of the reagents tested [adenosine 3',5' cyclic monophosphate (cAMP), guanosine 3',5y cyclic monophosphate (cGMP), inositol 1,4,5-trisphosphate (IP3), and diacylglycerol (DAG)] increased the tracer flux in vesicles or altered its response to GTP gamma S.

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39

Bell, Gordon M., Steven A. Atlas, Mark Pecker, Jean E. Sealey, Gary James, and John H. Laragh. "Diurnal and Postural Variations in Plasma Atrial Natriuretic Factor, Plasma Guanosine 3′:5′-Cyclic Monophosphate and Sodium Excretion." Clinical Science 79, no. 4 (October 1, 1990): 371–76. http://dx.doi.org/10.1042/cs0790371.

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1. We studied diurnal patterns of plasma atrial natriuretic factor, plasma guanosine 3′:5′-cyclic monophosphate and urinary sodium excretion in normal subjects after 3 days on a 200 mmol of sodium/60 mmol of potassium diet. On the fourth day blood samples and urine were collected every 3 h. 2. Two studies were performed. In study 1, normal subjects (n = 8) were recumbent for 23 h from 09.00 hours to 08.00 hours the next day. In study 2, normal subjects (n = 10) were permitted to ambulate from 09.00 hours to 23.00 hours and then were recumbent until 08.00 hours the next day. 3. In study 1, assumption of the recumbent posture was associated with increases in plasma atrial natriuretic factor (P < 0.01), plasma guanosine 3′:5′-cyclic monophosphate (P < 0.05) and urinary sodium excretion (P < 0.05). 4. In contrast, in study 2 there were no significant changes in plasma atrial natriuretic factor during the day; instead, plasma atrial natriuretic factor increased overnight, reaching a peak at 24.00 hours after 1 h of recumbency (P < 0.01). A smaller rise in plasma guanosine 3′:5′-cyclic monophosphate (P < 0.05) occurred; urinary sodium excretion decreased markedly (P < 0.01) and there was no change in creatinine clearance. 5. In both studies, recumbency was associated with an initial drop, followed by a rise, in packed cell volume. 6. These data demonstrate that assumption of the supine position induces a rise in plasma atrial natriuretic factor and accounts for most of the observed variation. This is associated with natriuresis during the day, but it does not reverse the pattern of antinatriuresis that occurs at night. Instead, changes in plasma atrial natriuretic factor appear to reflect and, in turn, influence changes in intravascular volume.

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40

Maeda, Hiroshi, Hiroshi Iranami, Manabu Yamamoto, Koji Ogawa, Yoshihiro Morikawa, Emiko Senba, and Yoshio Hatano. "Halothane but Not Isoflurane Attenuates Interleukin 1β– induced Nitric Oxide Synthase in Vascular Smooth Muscle." Anesthesiology 95, no. 2 (August 1, 2001): 492–99. http://dx.doi.org/10.1097/00000542-200108000-00035.

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Background Inducible nitric oxide synthase (iNOS) is induced by endotoxin or cytokines, such as interleukin (IL)-1, through a protein synthesis pathway. Halothane reportedly inhibits protein synthesis in various tissues. The aim of the current study was to examine the effect of halothane on the IL-1beta-evoked induction of NOS in vascular smooth muscle. Methods After removal of the endothelium, arterial rings of rat aorta were mounted in an isometric force recording system. The effects of halothane (1.0-3.0%) or isoflurane (3.0%) on IL-1beta (20 ng/ml)-induced inhibition of the contractile responses to KCl (30 mM) and phenylephrine (10(-9)-10(-5) M) were studied. The cyclic guanosine monophosphate and cyclic adenosine monophosphate contents were determined by radioimmunoassay. Expression of iNOS and iNOS mRNA were measured by Western or Northern blot analysis, respectively. Results Halothane (1.0-3.0%) but not isoflurane (3%) significantly reduced the ML-1beta-induced inhibition of contraction in a concentration-dependent manner. The cyclic guanosine monophosphate content of the vascular smooth muscle increased significantly after a 5-h exposure to IL-1beta. Halothane at 3.0% significantly inhibited the increase in cyclic guanosine monophosphate content induced by IL-1beta. Halothane had no effect on cyclic adenosine monophosphate content. IL-1beta-induced expression of iNOS and iNOS mRNA in the rat aorta were inhibited significantly by halothane. Conclusion The current study demonstrated that halothane but not isoflurane inhibits IL-1beta-stimulated hyporesponsiveness to vasoconstrictive agents in vascular smooth muscle and that this inhibitory effect of halothane involves the inhibition of iNOS mRNA expression. Thus, these findings suggest that halothane may have some sites to affect nitric oxide-signaling pathway.

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Zaffalon, F. G., C. Guimmelette, C. L. V. Leal, and F. J. Richard. "268 CYCLIC GUANOSINE MONOPHOSPHATE INHIBITS PHOSPHODIESTERASE 3 ACTIVITY IN PORCINE OOCYTES." Reproduction, Fertility and Development 25, no. 1 (2013): 282. http://dx.doi.org/10.1071/rdv25n1ab268.

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The level of cyclic adenosine monophosphate (cAMP) within oocytes has been shown to play a critical role in maintaining meiotic arrest. High levels of intracellular cAMP prevent spontaneous oocyte maturation in vitro, whereas a decrease in oocyte cAMP is associated with the resumption of meiosis. Another cyclic nucleotide that also was recently proposed as being involved in meiotic resumption is cyclic guanosine monophosphate (cGMP), which could be regulating phosphodiesterase (PDE) 3 activity. The aim of this study was to determine whether cGMP inhibits cAMP-PDE activity in porcine oocytes. With the method described previously by Sasseville et al. (2006 BMC Dev. Biol. 6, 47), PDE activity was measured in groups of 10 oocytes cultured in the absence (control) or presence of different concentrations of cGMP (1, 3, 10, 30, 100, 300, 1000, and 3000 nM) or with the PDE3 inhibitor cilostamide (10 µM). Before assaying PDE activity, the cumulus–oocyte complexes (COC) were matured in vitro for 24 h in the presence of pregnant mare serum gonadotropin (5 IU) and hCG (5 IU) at 38.5°C in 5% CO2. The COC were homogenised in a hypotonic buffer. Data were analysed using one-way ANOVA followed by Duncan’s post-hoc test. Differences with P < 0.05 were considered significant. Results showed that 300, 1000, and 3000 nM cGMP inhibited PDE3 activity (7.9, 5.1, and 4.1 fmol min–1 per COC; P < 0.05) at levels below the controls (13.2 fmol min–1 per COC) and were similar to the activity observed in the presence of (2.4 fmol min–1 per COC; P > 0.05). The other concentrations tested were similar to activity levels seen in the control (1 to 100 nM; 12.2, 11.3, 10.8, 11.5, and 10.4; P > 0.05). In conclusion, the results support the concept that increasing concentrations of cGMP inhibit PDE activity, suggesting the inhibition of the predominant form of cAMP-PDE present in porcine oocytes, PDE3. These results support the hypothesis that cGMP inhibits PDE activity in porcine oocytes. Further work is needed to determine the role this plays in maintaining high cAMP levels and inhibiting oocyte nuclear maturation. Financial support from FGZ FAPESP 2010/20188-6 and 2010/18023-9 is acknowledged.

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42

Lewis, Helen M., M. R. Wilkins, M. J. Kendall, and M. R. Lee. "Carbidopa Does Not Affect the Renal Response to Atrial Natriuretic Factor in Man." Clinical Science 77, no. 3 (September 1, 1989): 281–85. http://dx.doi.org/10.1042/cs0770281.

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1. The dependence of atrial natriuretic factor on renal dopamine for its renal effects in man was examined in 10 healthy volunteers using the dopa decarboxylase inhibitor carbidopa. 2. Each volunteer attended on two occasions, and received an infusion of atrial natriuretic factor (4 pmol min−1 kg−1) for 60 min after pretreatment with either placebo or carbidopa orally. These were administered in random, double-blind fashion. 3. A similar increase in plasma atrial natriuretic factor concentration was seen after atrial natriuretic factor infusion on both visits. 4. Infusion of atrial natriuretic factor produced a small unsustained rise in urinary dopamine excretion. This increase in urinary dopamine excretion was blocked by carbidopa with no effect on the natriuresis. 5. Urinary guanosine 3′:5′-cyclic monophosphate excretion increased in response to the atrial natriuretic factor infusion whether placebo or carbidopa was given. Guanosine 3′:5′-cyclic monophosphate, but not dopamine, may be a mediator of the renal response to atrial natriuretic factor in man.

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43

ERENMEMİŞOĞLU, Aydın, Cem SÜER, Sadun TEMOÇİN, and Hüseyin BEYDAĞI. "The Possible Role of 3':5'- Cyclic Guanosine Monophosphate in Acetylcholine-Mediated Concraction of Isolated Rat Duodenum." European Journal of Therapeutics 5, no. 1 (January 1, 1994): 16–20. http://dx.doi.org/10.58600/eurjther.1994-5-1-1369-arch.

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This study was planned to determine whether the possible role of 3':5'-cyclic guanosine monophosphate (cylic GMP) on acetylcholine(ACh) action in isolated rat duodenum. Therefore, sodium nitroprusside(SNP) and methylene blue(MB) were used as a guanylate cyclase activator and inhibitor respectively. MB caused significant fall in ACh-induced contraction peaks, whereas SNP did not alter them. These results suggested that cyclic GMP may play a role for ACh action in isolated duodenum smooth muscle. However further experiments are necessary to determine whether a causal relationship exists between cyclic GMP and ACh action.

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Antonenko, Yuri N., Alexander M. Firsov, Irina G. Rybalkina, Elena A. Kotova, Tatyana I. Rokitskaya, and Sergei D. Rybalkin. "The mitochondria-targeted antioxidant SkQ1 can carry adenosine 3′,5′-cyclic monophosphate, but not guanosine 3′,5′-cyclic monophosphate, through artificial and natural membranes." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1859 (September 2018): e113. http://dx.doi.org/10.1016/j.bbabio.2018.09.333.

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45

Ho, A. K., K. Hashimoto, and C. L. Chik. "3′,5′-Cyclic Guanosine Monophosphate Activates Mitogen-Activated Protein Kinase in Rat Pinealocytes." Journal of Neurochemistry 73, no. 2 (January 18, 2002): 598–604. http://dx.doi.org/10.1046/j.1471-4159.1999.0730598.x.

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46

Sato, M., K. Abe, K. Takeuchi, M. Yasujima, K. Omata, M. Hiwatari, Y. Kasai, M. Tanno, M. Kohzuki, and K. Kudo. "Atrial natriuretic factor and cyclic guanosine 3',5'-monophosphate in vascular smooth muscle." Hypertension 8, no. 9 (September 1986): 762–71. http://dx.doi.org/10.1161/01.hyp.8.9.762.

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47

Ohigashi, T., J. Brookins, and J. W. Fisher. "Interaction of nitric oxide and cyclic guanosine 3',5'-monophosphate in erythropoietin production." Journal of Clinical Investigation 92, no. 3 (September 1, 1993): 1587–91. http://dx.doi.org/10.1172/jci116740.

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48

Yamada, Hisafumi, Setsuro Hirai, Chiyo Suzuki-Hori, and Hiroshi Nagano. "Achromosomal cleavage of fertilized starfish eggs treated with cyclic guanosine 3′,5′-monophosphate." Journal of Experimental Zoology 235, no. 2 (August 1985): 247–53. http://dx.doi.org/10.1002/jez.1402350211.

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49

Reyes-Harde, Magali, Barry V. L. Potter, Antony Galione, and Patric K. Stanton. "Induction of Hippocampal LTD Requires Nitric-Oxide-Stimulated PKG Activity and Ca2+ Release From Cyclic ADP-Ribose-Sensitive Stores." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1569–76. http://dx.doi.org/10.1152/jn.1999.82.3.1569.

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Long-term depression (LTD) of synaptic transmission can be induced by several mechanisms, one thought to involve Ca2+-dependent activation of postsynaptic nitric oxide (NO) synthase and subsequent diffusion of NO to the presynaptic terminal. We used the stable NO donor S-nitroso- N-acetylpenicillamine (SNAP) to study the NO-dependent form of LTD at Schaffer collateral-CA1 synapses in vitro. SNAP (100 μM) enhanced the induction of LTD via a cascade that was blocked by the N-methyl-d-aspartate receptor antagonist d-2-amino-5-phosphonopentanoic acid (50 μM), NO guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (10 μM), and the PKG inhibitor KT5823 (1 μM). We further show that LTD induced by low-frequency stimulation in the absence of SNAP also is blocked by KT5823 or Rp-8-(4-chlorophenylthio)-guanosine 3′,5′-cyclic monophosphorothioate (10 μM), cyclic guanosine 3′,5′ monophosphate-dependent protein kinase (PKG) inhibitors with different mechanisms of action. Furthermore SNAP-facilitated LTD was blocked when release from intracellular calcium stores was inhibited by ryanodine (10 μM). Finally, two cell-permeant antagonists of the cyclic ADP-ribose binding site on ryanodine receptors also were able to block the induction of LTD. These results support a cascade for induction of homosynaptic, NO-dependent LTD involving activation of guanylyl cyclase, production of guanosine 3′,5′ cyclic monophosphate and subsequent PKG activation. This process has an additional requirement for release of Ca2+ from ryanodine-sensitive stores, perhaps dependent on the second-messenger cyclic ADP ribose.

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50

Bryan, R. M., M. L. Steenberg, M. Y. Eichler, T. D. Johnson, M. W. Swafford, and M. S. Suresh. "Permissive role of NO in alpha 2-adrenoceptor-mediated dilations in rat cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 3 (September 1, 1995): H1171—H1174. http://dx.doi.org/10.1152/ajpheart.1995.269.3.h1171.

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Dilations produced with UK-14304, a selective alpha 2-adrenoceptor agonist, in rat middle cerebral arteries (MCAs) were blocked after removal of the endothelium or inhibition of nitric oxide synthase (NOS). After endothelium removal or inhibition of NOS, the addition of subthreshold doses of an exogenous nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine, restored the dilations produced by UK-14304. In a similar manner the guanosine 3',5'-cyclic monophosphate (cGMP) analogues 8-bromoguanosine 3',5'-cyclic monophosphate and N2,2'-O-dibutyrylguanosine 3',5'-cyclic monophosphate restored the dilations of MCAs after endothelial removal. Because NO cannot be synthesized and released in MCAs after inhibition of NOS, it cannot be directly responsible for the dilation. The basal release of NO from the endothelium acts permissively in the vasodilation by maintaining adequate levels of cGMP. Removal of this basal release of NO by removal of endothelium or inhibition of NOS abolishes the alpha 2-adrenoceptor-mediated dilation.

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