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Aim To investigate the differences in the role of different purinergic receptor subtypes at different sites in postoperative-hyperalgesic priming in mice. Methods A postoperative-hyperalgesic priming model was constructed by injecting PGE
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In this article we review the relation between P2 purinoceptor subtypes and coronary heart disease (CHD).P2Y_1 ,P2Y_2 ,P2Y_(11) and P2X_7 receptors are related to inflammatory reaction in atheroselerosis plaque.P2X_3 receptor plays an important role in anginal nocuity response.P2X_4 receptor is involved in vascular remodeling and enhancement of myocardial contractility in non-infarct zone.P2Y2 and P2Y6 receptors are involved in resteno-sis.A polymorphism in P2Y_(11) receptors increase the risk of myocardial infarction.P2Y_1、P2Y_(12) and P2X_1 receptors play a role in thrombotic formation.The specific agonist and antagonist of P2 purinoceptor subtypes could be poten-tial targets for new drugs to treat CHD.
ABSTRACT
The discovery of non-adrenergic, non-cholinergic neurotransmission in the gut and bladder in the early 1960's is described as well as the identification of adenosine 5'-triphosphate (ATP) as a transmitter in these nerves in the early 1970's. The concept of purinergic cotransmission was formulated in 1976 and it is now recognized that ATP is a cotransmitter in all nerves in the peripheral and central nervous systems. Two families of receptors to purines were recognized in 1978, P1 (adenosine) receptors and P2 receptors sensitive to ATP and adenosine diphosphate (ADP). Cloning of these receptors in the early 1990's was a turning point in the acceptance of the purinergic signalling hypothesis and there are currently 4 subtypes of P1 receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of G protein-coupled receptors. Both short-term purinergic signalling in neurotransmission, neuromodulation and neurosecretion and long-term (trophic) purinergic signalling of cell proliferation, differentiation, motility, death in development and regeneration are recognized. There is now much known about the mechanisms underlying ATP release and extracellular breakdown by ecto-nucleotidases. The recent emphasis on purinergic neuropathology is discussed, including changes in purinergic cotransmission in development and ageing and in bladder diseases and hypertension. The involvement of neuron-glial cell interactions in various diseases of the central nervous system, including neuropathic pain, trauma and ischemia, neurodegenerative diseases, neuropsychiatric disorders and epilepsy are also considered.
Subject(s)
Animals , Humans , Adenosine Triphosphate/physiology , Central Nervous System Diseases/physiopathology , Neurotransmitter Agents/physiology , Receptors, Purinergic/physiology , Signal Transduction/physiologyABSTRACT
Purinergic receptors are divided into P1(adenosine)and P2(ATP)receptors.P2 receptor are divided into two subtypes,namely P2X(ligand-gated ion channels)and P2Y(G-protein coupled)receptors.Several kinds of purinoceptor subtypes have been expressed in endocrine pancreas and participate in regulating the secretion of insulin.Purinoceptor and ligand are correlated with pathogenesis of diabetes mellitus and complications and make it possible to provide a new target to treat diabetes mellitus and complications.
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We explore the question of whether adenosine 5'-triphosphate (ATP) acts as an excitatory neurotransmitter in guinea-pig gastric smooth muscle. In an organ bath system, isometric force of the circular smooth muscle of guinea-pig gastric antrum was measured in the presence of atropine and guanethidine. Under electrical field stimulation (EFS) at high frequencies (>20 Hz), NO-mediated relaxation during EFS was followed by a strong contraction after the cessation of EFS (a "rebound-contraction"). Exogenous ATP mimicked the rebound-contraction. A known P2Y-purinoceptor antagonist, reactive blue 2 (RB-2), blocked the rebound-contraction while selective desensitization of P2x-purinoceptor with alpha, beta-MeATP did not affect it. ATP and 2-MeSATP induced smooth muscle contraction, which was effectively blocked by RB-2 and suramin, a nonselective P2-purinoceptor antagonist. Particularly, in the presence of RB-2, exogenous ATP and 2-MeSATP inhibited spontaneous phasic contractions, suggestingthe existence of different populations of purinoceptors. Both the rebound-contraction and the agonist-induced contraction were not inhibited by indomethacin. The rank orders of agonists' potency were 2-MeSATP > ATP gtoreq UTP for contraction and alpha, beta-MeATP gtoreq beta, gamma-MeATP for inhibition of the phasic contraction, that accord with the commonly accepted rank order of the classical P2Y-purinoceptor subtypes. Electrical activities of smooth muscles were only slightly influenced by ATP and 2-MeSATP, whereas alpha, beta-MeATP attenuated slow waves with membrane hyperpolarization. From the above results, it is suggested that ATP acts as an excitatory neurotransmitter, which mediates the rebound-contraction via P2Y-purinoceptor in guinea-pig gastric antrum.