Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The responses of the guinea-pig taenia coli, urinary bladder, and the rabbit portal vein to ultraviolet (u.v.) light were compared to those elicited by purinergic nerve stimulation and exogenous adenosine triphosphate (ATP).2 In the presence of sodium nitrite, u.v. light between 340-380 nm produced a maximum relaxation of the taenia coli. The relaxation was reversible and fast in onset. It was unaffected by atropine, guanethidine or low concentrations of phentolamine or propranolol. When the tone was low, the relaxation was usually followed by a ;rebound contraction' upon cessation of stimulation. Thus, the response to u.v. light closely resembles the responses to both purinergic nerve stimulation and exogenously applied ATP.3 U.v. light did not initiate impulses in purinergic nerves since its action was unaffected by tetrodotoxin; nor did it release ATP from nerve terminals (in contrast to its release during purinergic nerve stimulation). The adenosine-uptake inhibitor, dipyridamole, which potentiates the responses to purinergic nerve stimulation and ATP, did not affect the response to u.v. light.4 Agents known to alter postjunctional responses to purinergic nerve stimulation and ATP also altered the response to u.v. light. High concentrations of the 2-substituted imidazoline compounds, antazoline and phentolamine, which antagonize the responses to purinergic nerve stimulation and ATP, reduced the responses to u.v. irradiation. The prostaglandin synthesis inhibitor, indomethacin, which abolishes the ;rebound contraction' following stimulation of purinergic nerves, also blocks the ;rebound ;contraction' following u.v. irradiation. Increases in the K(+) concentration produced parallel changes in the inhibitory responses to u.v. light and purinergic nerve stimulation.5 U.v. light produced relaxation and inhibition of spontaneous activity of the rabbit portal vein (relaxed by ATP), but had no effect on the guinea-pig urinary bladder (contracted by ATP) and ureter (unaffected by ATP).6 It is suggested that u.v. light is acting on some part of the purinergic receptor complex which is involved in the mediation of inhibitory responses to ATP and purinergic nerve stimulation, and may therefore provide a way of investigating the chemistry of inhibitory purinergic receptors.
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PMID:Comparison of the effects of ultraviolet light and purinergic nerve stimulation on the guinea-pig taenia coli. 62 41

Adenosine 5'-triphosphate (ATP) mediates a variety of biological functions and has been shown to play a physiological role in almost every system in the body. In the genito-urinary system, extracellular ATP has been shown to play a functional role in several different capacities, ranging from nociception in the ureter and bladder, to erectile dysfunction via its action on different 'purinergic receptors'. Discovery of the trophic effects of ATP has led to a surge in interest in this signalling system in various malignancies. To date five P2 receptor subtypes have been implicated in the growth inhibition of cancer cells, namely P2X5, P2X7, P2Y1, P2Y2 and P2Y11. Limited data are available on urological malignancies. ATP induces its anti-neoplastic effect primarily via purinergic receptor-mediated apoptosis via calcium-independent pathways, and this has been confirmed in vitro and in vivo. Studies have highlighted functional roles for the P2X5 and/or P2Y11 receptors in both hormone refractory prostate cancer and high-grade bladder cancer, although the contributory effect of pro-apoptotic P2X7 receptors remains unclear. Clinical trials have shown intravenous ATP successfully attenuates a range of systemic symptoms associated with advanced malignancies. This raises the possibility that selective targeting of specific aberrant pathways may allow for treatment of advanced primary malignancies and their systemic effects.
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PMID:Purinergic receptor-mediated effects of adenosine 5'-triphosphate in urological malignant diseases. 1918 33