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

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

doi:10.1111/j.1476-5381.1994.tb14782.x

Cited by 11 publications

(4 citation statements)

References 28 publications

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“…Moreover, Rp-cAMP, an inhibitor of adenosine 3« ,5« -monophosphate-dependent protein kinase A (Wang et al 1991), suppressed the noradrenaline-releasing action of paeoni¯orin ( Figure 4) within a concentration range eOE ective at blocking the action of cyclic AMP (Murthy et al 1995). It has been documented that cyclic AMP is involved in the release of neurotransmitter (Ouedraogo et al 1994). The results we obtained are consistent with this and show that paeoni¯orin induced a calcium-dependent and cyclic-AMP-related release of noradrenaline from noradrenergic terminals of guinea-pig ileum.…”

Section: Discussionsupporting

confidence: 92%

Stimulatory effect of paeoniflorin on the release of noradrenaline from ileal synaptosomes of guinea-pig in-vitro

Liu

Tsai

et al. 2002

Journal of Pharmacy and Pharmacology

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The effect of paeoniflorin (an active principle of Paeoniae Radix, commonly used in traditional Chinese medicine) on the release of noradrenaline (norepineprhine) from nerve terminals was investigated using guinea-pig isolated ileal synaptosomes. Release was determined as the amount of noradrenaline, quantified by high-performance liquid chromatography-electrochemical detection, from samples incubated with paeoniflorin or vehicle. Paeoniflorin stimulated the release of noradrenaline in a concentration-dependent manner without an effect on the level of lactate dehydrogenase in the bathing medium. Tetrodotoxin abolished the action of paeoniflorin at concentrations sufficient to block sodium channels. The depolarizing effect of paeoniflorin on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol. Moreover, the effect of paeoniflorin on bisoxonol fluorescence in ileal synaptosomes seems more potent than that of 4-aminopyridine. That paeoniflorin causes influx of calcium ions via the depolarization of nerve terminals could be considered. The noradrenaline-releasing action of paeoniflorin was abolished by removal of calcium chloride from the bathing medium. This action of paeoniflorin was also attenuated by Rp-cAMP atconcentrations sufficientto inhibitthe action of cyclicAMP. Therefore, paeoniflorin could induce a calcium-dependent and cyclic-AMP-related release of noradrenaline from sympathetic nerve terminals of guinea-pig ileum. Guanethidine inhibited the noradrenaline-releasing action of paeoniflorin in a concentration-dependent manner. The effect of paeoniflorin on the increase of bisoxonol fluorescence was not modified by atropine. Release of noradrenaline by paeoniflorin from noradrenergic nerve terminals was characterized. These findings suggest that paeoniflorin can stimulate tetrodotoxin-sensitive depolarization of membranes to result in a calcium-dependent and cyclic-AMP-related release of noradrenaline from noradrenergic nerve terminals.

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Section: Discussionsupporting

confidence: 92%

Stimulatory effect of paeoniflorin on the release of noradrenaline from ileal synaptosomes of guinea-pig in-vitro

Liu

Tsai

et al. 2002

Journal of Pharmacy and Pharmacology

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“…The selectivity towards PKG is also confirmed in the present functional studies. Activation of PKA has been implicated in the enhancing effect of cyclic AMP-elevating compounds on prejunctional release of noradrenaline (Ouedraogo et al, 1994a) and in the present study, forskolin induced a concentration-dependent vasodilator effect on preconstricted arteries. Both effects which are assumed to operate via activation of PKA (reviewed by Beebe & Corbin, 1986) are unaffected by (Rp)-8-bromo-PET-cycic GMPS at a concentration which produced an inhibition of effects involving the cyclic GMP/ PKG-operated pathway.…”

Section: Functional Studiessupporting

confidence: 71%

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

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104

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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.

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“…The effects of the two 8-substituted analogues of cyclic GMP on stimulation-induced noradrenaline release were inhibited by the selective PKA inhibitor H-89 (Chijiwa et al, 1990), suggesting an involvement of PKA. In the same experimental model H-89 significantly attenuates the enhancement of electrically-evoked release of [3H]-noradrenaline by forskolin, isoprenaline and 8-bromo-cyclic AMP (Ouedraogo et al, 1994). The cyclic GMP analogue PET-cyclic GMP, which had no effect on transmitter release is 10 to 20 times less potent in activating PKA than 8-bromo-cyclic GMP and 8-pCPT-cyclic GMP (Francis et al, 1988).…”

Section: Discussionmentioning

confidence: 98%

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

Ouédraogo¹,

Stoclet²,

Bucher³

1994

British J Pharmacology

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1 The effects of membrane permeable analogues of guanosine 3':5'-cyclic monophosphate (cyclic GMP), and of the NO donor, 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1) were investigated on [3H]-noradrenaline release and neurogenic vasoconstriction in electrical field stimulated rat tail arteries. 2 Two 8-substituted analogues of cyclic GMP (8-bromoguanosine 3':5'-cyclic monophosphate; 8-bromo-cyclic GMP and 8-(4-chlorophenylthio)-guanosine 3':5'-cyclic monophosphate; 8-pCPT-cyclic GMP) concentration-dependently enhanced stimulation-induced [3H]-noradrenaline release. These prejunctional effects were antagonized by the cyclic AMP-dependent protein kinase (PKA) inhibitor N-[2-((3-(4-bromophenyl)-2-propenyl)-amino)-ethyl]-5 isoquinolinesulphonamide dihydrochloride (H-89; 100 nM) but not by the cyclic GMP-dependent protein kinase (PKG) inhibitors, Rp-8-bromoguanosine 3':5'-cyclic monophosphorothioate (Rp-8-bromo-cyclic GMPS; 10I M) or Rp-8-(4-chlorophenylthio)-guanosine 3':5'-cyclic monophosphorothioate (Rp-8-pCPT-cyclic GMPS; 1O pM).3 P-Phenyl-l,N2-ethenoguanosine 3':5'-cyclic monophosphate (PET-cyclic GMP) had no effect on stimulation-induced [3H]-noradrenaline release but concentration-dependently decreased the stimulationinduced vasoconstriction. 4 The two 8-substituted cyclic GMP derivatives, PET-cyclic GMP and SIN-1, both decreased stimulation-induced vasoconstriction. In addition, SIN-1 relaxed rat tail arteries precontracted with phenylephrine (1 JAM). The SIN-i concentration-relaxation curve was shifted in parallel manner to the right by Rp-8-bromo-cyclic GMPS (10 JAM) and Rp-8-pCPT-cyclic GMPS (10 rM) with no change in the maximum effect, showing that the relaxation was mediated by a cyclic GMP/PKG-dependent mechanism. 5It is concluded that PKA activation is involved in the noradrenaline release enhancing effect of the two 8-substituted cyclic GMP analogues, whereas a cyclic GMP/PKG-operated pathway accounts for the inhibitory effects of the cyclic GMP and its analogues on vascular smooth muscle contraction.

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

Cited by 11 publications

References 28 publications

Stimulatory effect of paeoniflorin on the release of noradrenaline from ileal synaptosomes of guinea-pig in-vitro

Stimulatory effect of paeoniflorin on the release of noradrenaline from ileal synaptosomes of guinea-pig in-vitro

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

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

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