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Possible Interaction: Adenosine and Capsaicin

supplement:

Adenosine

supplement:

Capsaicin

Research Papers that Mention the Interaction

Adenosine release is reduced by intrathecal and neonatal pretreatment with capsaicin but not by intrathecal pretreatment with 6-hydroxydopamine or 5,7-dihydroxytryptamine, indicating that adenosine originates from small-diameter primary afferent neurons but not descending monoaminergic pathways.
Trends in pharmacological sciences  •  1989  |  View Paper
Results: Adenosine , in the concentration of 100 µM, injected into the femoral artery had an inhibitory effect on the reflex RSNA and BP responses induced by capsaicin.
Cellular Physiology and Biochemistry  •  2016  |  View Paper
The inhibition of AMP‐ and CPA‐induced airway obstruction by atropine, capsaicin and bilateral vagotomy suggests a neuronal‐dependent mechanism with the particular involvement of capsaicin‐sensitive nerves.
British journal of pharmacology  •  2006  |  View Paper
Pretreatment with lidocaine, the β-receptor agonist, terbutaline, or the adenosine non-blocking xanthine, enprofylline, inhibited the capsaicine induced inflammatory response.
Agents and Actions  •  2005  |  View Paper
Systemic pretreatment with capsaicin , a neurotoxin selective for small-diameter sensory afferents, markedly reduced the saline-evoked release of adenosine in rat hind paw following spinal nerve ligation.
Neuroscience  •  2002  |  View Paper
Acute injection of 1% capsaicin to the hind paw of untreated rats also induced adenosine release.
Pretreatment with capsaicin , a neurotoxin selective for unmyelinated small diameter primary afferent nerves, markedly reduced the adenosine released by 1.5% formalin and the early phase of release by 5% formalin.
European journal of pharmacology  •  2001  |  View Paper
In rats treated with capsaicin to destroy sensory neurons, the response to higher doses of adenosine , CPA and NECA, but not IB‐MECA, was significantly inhibited.
British journal of pharmacology  •  2001  |  View Paper
Adenosine (1-10 microM) … dose dependently the capsaicin 10 microM)-induced depolarization of myenteric neurons, but did not inhibit the depolarizing response to exogenous substance P. The adenosine P1 receptor antagonist, 8-phenyltheophylline (1-10 microM), antagonized the inhibitory effect of adenosine (1-10 microM) on the mechanical responses.
Adenosine (10-100 microM) suppressed the contractile response to a threshold concentration of capsaicin (1 microM) while leaving the contractile response to a submaximal concentration of substance P (1 nM) and acetylcholine (0.1 microM) intact.
European journal of pharmacology  •  1993  |  View Paper
Calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine mimicked the inhibitory action of capsaicin on nerve stimulation in all groups, while substance P was without effect.
These results suggest that senna or its metabolites may cause a sensory neuropathy of mesenteric resistance vessels and that calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine , but not substance P, are possible candidates as mediators of the inhibitory effects induced by capsaicin.
Gastroenterology  •  1990  |  View Paper
Exposure of dorsal, but not ventral, spinal cord synaptosomes to capsaicin produced a dose- and Ca++-dependent release of adenosine , which was reduced by capsaicin pretreatment (neonatal and adult) and inhibition of ecto-5'-nucleotidase.
Intrathecal capsaicin also inhibited morphine-evoked release of adenosine in vivo.
The Journal of pharmacology and experimental therapeutics  •  1989  |  View Paper
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