Effects of cyclic GMP and analogues on neurogenic transmission in the rat tail artery

Ouédraogo, Sylvin; Stoclet, Jean‐Claude; Bucher, Bernard

doi:10.1111/j.1476-5381.1994.tb13160.x

Cited by 16 publications

(7 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among the cyclic GMP analogues described in previous studies, 8-bromo-PET-cyclic GMP is one of the most potent smooth muscle relaxing agents, presumably acting via the activation of PKG (Sekhar et al, 1992). This cyclic GMP analogue decreases the vasoconstrictor response in a concentration-dependent fashion without affecting nerve-induced neurotransmitter release, in agreement with our previous observations with other analogues (Ouedraogo et al, 1994b). The relaxation induced by the NO donor SIN-I which activates guanylyl cyclase (B6hme et al, 1984) is thought to be mediated by the endogenous production of cyclic GMP which then activates PKG.…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Inhibition of cyclic GMP‐dependent protein kinase‐mediated effects by (Rp)‐8‐bromo‐PET‐cyclic GMPS

Butt¹,

Pöhler²,

Genieser

et al. 1995

British J Pharmacology

Self Cite

104

View full text Add to dashboard Cite

1 The modulation of the guanosine 3':5'-cyclic monophosphate (cyclic GMP)-and adenosine 3':5'-cyclic monophosphate (cyclic AMP)-dependent protein kinase activities by the diastereomers of 8-bromoflphenyl-1,N2-ethenoguanosine 3',5'-cyclic monophosphorothioate, ((Rp)-and (Sp)-8-bromo-PET-cyclic GMPS) was investigated by use of purified protein kinases. In addition, the effects of (Rp)-8-bromo-PET-cyclic GMPS on protein phosphorylation in intact human platelets and on [3H]-noradrenaline release and neurogenic vasoconstriction in electrical field stimulated rat tail arteries were also studied. 6 The NO donor, 3-morpholinosydnonimine (SIN-1) relaxed rat tail arteries precontracted with phenylephrine (1 gM). The SIN-1 concentration-relaxation curve was shifted in a parallel manner to the right by (Rp)-8-bromo-PET-cyclic GMPS, suggesting that the relaxation was mediated by a cyclic GMP/ PKG-dependent mechanism. 7 The [3H]-noradrenaline release-enhancing effect and stimulation-induced decrease in vasoconstriction of forskolin were unaffected by (Rp)-8-bromo-PET-cyclic GMPS. Moreover, the forskolin concentrationrelaxation curve was not changed in the presence of the PKG inhibitor, suggesting a high selectivity in intact cells for PKG-over PKA-mediated effects.8 The results obtained indicate that (Rp)-8-bromo-PET-cyclic GMPS presently is the most potent and selective inhibitor of PKG and is helpful in distinguishing between cyclic GMP and cyclic AMP messenger pathways activation. Therefore, this phosphorothioate stereomer may be a useful tool for studying the role of cyclic GMP in vitro.

show abstract

Section: Discussionsupporting

confidence: 89%

“…RT-PCR studies Our recent studies with cyclic nucleotide analogues suggest that the postjunctional action of cyclic GMP in rat tail artery involves the activation of PKG la and probably IB (Ouedraogo et al, 1994b). Therefore, we investigated the presence of PKG mRNA in this tissue.…”

Section: Biochemical Studiesmentioning

confidence: 99%

Inhibition of cyclic GMP‐dependent protein kinase‐mediated effects by (Rp)‐8‐bromo‐PET‐cyclic GMPS

Butt¹,

Pöhler²,

Genieser

et al. 1995

British J Pharmacology

Self Cite

104

View full text Add to dashboard Cite

show abstract

“…However, a number of cGMP analogues as well as cGMP itself activate protein kinase A (Miller et al, 1981;Ogreid et al, 1989;Cornwell et al, 1994;Ouedraogo et al, 1994). Addition of analogs of cAMP, known to activate protein kinase A, can enhance the neuritogenic effects of NGF in PC12 cells (Gunning, 1981b).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide donors enhance neurotrophin-induced neurite outgrowth through a cGMP-dependent mechanism

et al. 1997

View full text Add to dashboard Cite

Nitric oxide (NO), a diffusible and unstable gas, has been implicated in inter‐ and intra‐cellular communication in the nervous system. NO also plays a role in neural development, plasticity and alterations of synaptic function such as long‐term potentiation and long‐term depression (Gally et al.: Proc NY Acad Sci, 87:354–355, 1990; Zhuo et al.: Science 260:1946–1950, 1993; Schuman and Madison.: Science 254:1503–1506, 1991; Bruhwyler et al.: Neurosci Biobehav Rev 17:373–384, 1993) some of which likely involve growth and remodelling of neurites. Some actions of NO are mediated directly by protein modification (e.g., nitrosylation) and others by activation of soluble guanylyl cyclase (soluble GC), which increases intracellular levels of guanosine 3′,5′‐cyclic monophosphate (cGMP). NO is synthesized by the enzyme nitric oxide synthase (NOS), which is induced by treatment of CNS neurons (Holtzman et al.: Neurobiol Disease 1:51–60, 1994) or pheochromocytoma PC12 cells (Hirsch et al.: Curr Biol 3:749–754, 1993) with NGF. NO has been proposed to mediate some of the effects of NGF on PC12 cells by inhibiting cell division (Peunova and Enikolopov: Nature 374:68–73, 1995). In addition, NO can substitute for NGF by delaying the death of trophic factor‐deprived PC12 cells through a mechanism that does not involve a cytostatic action (Farinelli et al.: J Neurosci 16:2325–2334, 1996). We investigated whether NO stimulated neurite outgrowth from hippocampal neurons and PC12 cells. Primary cultures of E17 mouse hippocampal neurons co‐cultured with neopallial astrocytes were exposed to the NO donors sodium nitrite (100 μM) or sodium nitroprusside (100 nM). After 48 hr, NO donor‐treated cultures contained a greater proportion of cells bearing neurites and neurites that were much longer than those found in control cultures. In cultures of PC12 cells, NO donors also enhanced the neuritogenic effects of NGF. The proportion of PC12 cells with neurites 48 hr after exposure to NO donors sodium nitrite (100 μM–10 mM) or sodium nitroprusside (100 nM–1 μM) plus 2.5S nerve growth factor (NGF) was approximately twice the proportion of cells with neurites in sister cultures grown in NGF alone. Neither of the NO donors elicited neurites from the PC12 cells in the absence of NGF. The effects of the NO donors were likely mediated by release of NO since their effects were antagonized by addition of hemoglobin, which avidly binds NO, to the culture medium. The enhancement by NO of NGF‐mediated neurite outgrowth in PC12 cells appeared to occur through a cGMP‐dependent mechanism. The NO donors stimulated a prompt increase in intracellular cGMP in PC12 cells. Moreover their action was mimicked by addition of the membrane‐permeant cGMP analogs 8‐Bromo‐cGMP (8‐Br‐cGMP) and para (chlorophenylthio)‐cGMP (pCPT‐cGMP) to the culture medium and by atrial natriuretic factor which stimulates particulate guanylyl cyclase. The neuritogenic activity of the NO donors was inhibited by LY83583 and methylene blue, inhibitors of guanylyl cyclase. These data i...

show abstract

“…F9 cells were treated with 8-BrcGMP to activate and with Rp-8-(4-chlorophenylthio)-guanosine 3Ј:5Ј-cyclic monophosphorothioate (Rp-8-pCPT-cyclic GMP) to inhibit PKG (23), and Ca 2ϩ mobilization was monitored (Fig. 4C).…”

Section: Efficiency Of Knockdown Of G-protein Subunits Targeted By Anmentioning

confidence: 99%

Suppression of Cyclic GMP-dependent Protein Kinase Is Essential to the Wnt/cGMP/Ca2+ Pathway

Wang

2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

Effects of cyclic GMP and analogues on neurogenic transmission in the rat tail artery

Cited by 16 publications

References 57 publications

Inhibition of cyclic GMP‐dependent protein kinase‐mediated effects by (Rp)‐8‐bromo‐PET‐cyclic GMPS

Inhibition of cyclic GMP‐dependent protein kinase‐mediated effects by (Rp)‐8‐bromo‐PET‐cyclic GMPS

Nitric oxide donors enhance neurotrophin-induced neurite outgrowth through a cGMP-dependent mechanism

Suppression of Cyclic GMP-dependent Protein Kinase Is Essential to the Wnt/cGMP/Ca2+ Pathway

Contact Info

Product

Resources

About