The role of purines in nociception

Sawynok, Jana; Sweeney, Marva I.

doi:10.1016/0306-4522(89)90278-9

Cited by 192 publications

(55 citation statements)

References 101 publications

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“…In spinal cord, serotonin (5-HT) has been shown to release a nucleotide from dorsal horn spinal cord synaptosomes that is degraded extracellularly to adenosine, leading to the hypothesis that this mechanism might in part underlie the antinociception produced by 5-HT (DeLander and Hopkins, 1987;Sweeney et al, 1988;Sawynok and Sweeney, 1989). Sweeney et al (1990) present evidence that this nucleotide is, in fact, CAMP.…”

Section: Discussionmentioning

confidence: 98%

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Knowles

et al. 1994

J. Neurosci.

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Adenosine is an important inhibitory neuromodulator in the CNS, yet the sources of extracellular adenosine have yet to be well characterized. In this study we show that beta-adrenergic stimulation of cortical cultures results in the extracellular accumulation of cAMP as well as adenosine, and that the extracellular adenosine derives from extracellular cAMP. The concentration dependence of isoproterenol in evoking cAMP secretion was determined by radioimmunoassay, and the EC50 for this effect was found to be approximately 100 nM. In order to investigate the effect of beta-adrenergic stimulation on the regulation of extracellular adenosine, the effect of isoproterenol in stimulating the extracellular accumulation of adenine-containing compounds was examined by HPLC. Isoproterenol stimulated cAMP secretion in both astrocyte cultures and astrocyte-rich mixed cultures of astrocytes and neurons. However, no extracellular cAMP was detectable in neuron- enriched astrocyte-poor cultures. Extracellular adenosine increased in response to isoproterenol in the astrocyte-rich mixed cultures, but not in the neuron-enriched astrocyte-poor cultures. After 30 min exposure to isoproterenol, the concentration of adenosine in the extracellular medium increased by 47% in 56 experiments in the mixed astrocyte-rich cultures. In order to establish whether the adenosine that accumulates in response to isoproterenol stimulation actually derives from extracellular cAMP, phosphodiesterase inhibitors were tested for their ability to block isoproterenol-stimulated adenosine accumulation. Isobutylmethylxanthine (IBMX; 100 microM), RO 20–1724 (180 microM), carbazeran (10 microM), dipyridamole (10 microM), and trifluoperazine (10 microM) had no inhibitory effect on the isoproterenol-stimulated accumulation of extracellular adenosine. However 100 microM IBMX plus 180 microM RO 20–1724 effectively blocked isoproterenol-stimulated adenosine accumulation and, as expected, increased extracellular cAMP. As a further test of the origin of isoproterenol-stimulated adenosine accumulation, we attempted to block this phenomenon by blocking cAMP secretion itself. For this purpose probenecid, a known inhibitor of cAMP secretion in many different cell types, was used. We found that probenecid at 1 mM blocked isoproterenol-stimulated adenosine accumulation. These studies suggest that one potentially important source of extracellular adenosine in the cerebral cortex is endogenous extracellular cAMP, secreted from astrocytes in response to beta- adrenergic receptor stimulation. Since the receptors of neuromodulators other than norepinephrine may also be coupled to adenylyl cyclase in the cerebral cortex, there may be several neuromodulatory systems that regulate extracellular adenosine levels by this mechanism.

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Section: Discussionmentioning

confidence: 98%

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Knowles

et al. 1994

J. Neurosci.

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“…First, ATP is carried in red blood cells and when oxygen concentration is low in a working muscle region, the red blood cell deforms, resulting in a cascade of events that lead to ATP release via pannexin channels [5,6]. Once released, ATP binds to purinergic (P2X and P2Y) receptors on endothelial cells [7,8]. Binding results in the endothelial cells releasing nitric oxide via endothelial nitric oxide synthase, prostacyclin, and endothelium-derived hyperpolarizing factor [28], all 3 of which affect the smooth muscle of the vasculature via cyclic guanosine monophosphate, cyclic adenosine monophosphate, and hyperpolarization, respectively [5].…”

Section: Effects Of Atp Supplementation On Peak Power and Muscle Excimentioning

confidence: 99%

“…In addition, ATP has extensive extracellular functions that are primarily mediated through purinergic (P2Y and P2X) membrane receptors ubiquitously present in many cell types [5,6]. Extracellular-mediated functions of ATP include the increase in skeletal muscle calcium permeability, the blocking of chloride efflux, and vasodilation [7,8]. ATP is a food ingredient and part of our daily diet, with meat, fish, and nuts being particularly good sources.…”

Section: Introductionmentioning

confidence: 99%

Oral Adenosine-5′-triphosphate (ATP) Administration Increases Postexercise ATP Levels, Muscle Excitability, and Athletic Performance Following a Repeated Sprint Bout

Purpura¹,

Rathmacher

Sharp

et al. 2017

Journal of the American College of Nutrition

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Objective: Oral adenosine-5 0 -triphosphate (ATP) administration has failed to increase plasma ATP levels; however, chronic supplementation with ATP has shown to increase power, strength, lean body mass, and blood flow in trained athletes. The purpose of this study was to investigate the effects of ATP supplementation on postexercise ATP levels and on muscle activation and excitability and power following a repeated sprint bout. Methods: In a double-blind, placebo-controlled, randomized design, 42 healthy male individuals were given either 400 mg of ATP as disodium salt or placebo for 2 weeks prior to an exercise bout. During the exercise bout, muscle activation and excitability (ME, ratio of power output to muscle activation) and Wingate test peak power were measured during all sprints. ATP and metabolites were measured at baseline, after supplementation, and immediately following exercise. Results: Oral ATP supplementation prevented a drop in ATP, adenosine-5 0 -diphosphate (ADP), and adenosine-5 0 -monophosphate (AMP) levels postexercise (p < 0.05). No group by time interaction was observed for muscle activation. Following the supplementation period, muscle excitability significantly decreased in later bouts 8, 9, and 10 in the placebo group (¡30.5, ¡28.3, and ¡27.9%, respectively; p < 0.02), whereas ATP supplementation prevented the decline in later bouts. ATP significantly increased Wingate peak power in later bouts compared to baseline (bout 8: C18.3%, bout 10: C16.3%). Conclusions: Oral ATP administration prevents exercise-induced declines in ATP and its metabolite and enhances peak power and muscular excitability, which may be beneficial for sports requiring repeated high-intensity sprinting bouts.

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“…N 6 -(2-hydroxyethyl) adenosine (HEA), an adenosine derivative, is one of the main bioactive ingredients from C. cicadae. Since 1980s, researchers have confirmed that endogenous nucleosides and their analogues may be involved in pain modulation [10,11]. HEA can bind to α1 receptors, thereby exerting an analgesic effect by inhibiting neurotransmitter release [12].…”

Section: Introductionmentioning

confidence: 99%

Prenatal Developmental Toxicity Study of HEA-enriched Cordyceps Cicadae Mycelia in Sprague-Dawley Rats

Li¹

2017

JFST

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The role of purines in nociception

Cited by 192 publications

References 101 publications

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Oral Adenosine-5′-triphosphate (ATP) Administration Increases Postexercise ATP Levels, Muscle Excitability, and Athletic Performance Following a Repeated Sprint Bout

Prenatal Developmental Toxicity Study of HEA-enriched Cordyceps Cicadae Mycelia in Sprague-Dawley Rats

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