Inhibition of purinergic transmission by prostaglandin E1 and E2 in the guinea‐pig vas deferens: an electrophysiological study

1 The effects of prostaglandin E1 (PGE1) and E2 (PGE2) on postjunctional electrical activity in the guinea‐pig vas deferens evoked by sympathetic nerve stimulation were investigated using both intracellular and focal extracellular recording techniques in vitro. 2 Bath application of PGE1 (1–100 nM)...

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Veröffentlicht in:British journal of pharmacology 1996-06, Vol.118 (3), p.776-782
Hauptverfasser: Brock, James A., Cunnane, Thomas C.
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description 1 The effects of prostaglandin E1 (PGE1) and E2 (PGE2) on postjunctional electrical activity in the guinea‐pig vas deferens evoked by sympathetic nerve stimulation were investigated using both intracellular and focal extracellular recording techniques in vitro. 2 Bath application of PGE1 (1–100 nM) or PGE2 (0.1–100 nM) concentration‐dependently inhibited the amplitudes of all excitatory junction potentials (e.j.ps) evoked during short trains of stimuli (10 stimuli at 1 Hz). Increasing the duration of nerve stimulation (100 stimuli at 1 Hz) did not overcome this inhibitory effect. At these concentrations PGE1 and PGE2 were without any apparent inhibitory effect on the amplitudes of spontaneous e.j.ps. 3 Local application of PGE1 (10–100 nM) or PGE2 (10–30 nM) markedly reduced the frequency of occurrence of excitatory junction currents (e.j.cs) evoked by trains of 20–100 stimuli at 1 to 4 Hz without changing the amplitudes of spontaneous e.j.cs or the configuration of the nerve terminal impulse. 4 In the presence of PGE1 or PGE2, raising the frequency of stimulation (from 1 to 4 Hz), increased the likelihood of e.j.c. occurrence. 5 The postjunctional electrical activity recorded in the guinea‐pig vas deferens is believed to be due to ATP released from the sympathetic nerve endings. Thus the present study demonstrates that both PGE1 and PGE2 powerfully inhibit quantal ATP release in the guinea‐pig vas deferens.
doi_str_mv 10.1111/j.1476-5381.1996.tb15467.x
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Increasing the duration of nerve stimulation (100 stimuli at 1 Hz) did not overcome this inhibitory effect. At these concentrations PGE1 and PGE2 were without any apparent inhibitory effect on the amplitudes of spontaneous e.j.ps. 3 Local application of PGE1 (10–100 nM) or PGE2 (10–30 nM) markedly reduced the frequency of occurrence of excitatory junction currents (e.j.cs) evoked by trains of 20–100 stimuli at 1 to 4 Hz without changing the amplitudes of spontaneous e.j.cs or the configuration of the nerve terminal impulse. 4 In the presence of PGE1 or PGE2, raising the frequency of stimulation (from 1 to 4 Hz), increased the likelihood of e.j.c. occurrence. 5 The postjunctional electrical activity recorded in the guinea‐pig vas deferens is believed to be due to ATP released from the sympathetic nerve endings. Thus the present study demonstrates that both PGE1 and PGE2 powerfully inhibit quantal ATP release in the guinea‐pig vas deferens.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1996.tb15467.x</identifier><identifier>PMID: 8762107</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenosine Triphosphate - metabolism ; Alprostadil - pharmacology ; Animals ; ATP ; Biological and medical sciences ; Dinoprostone - pharmacology ; electrophysiology ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; In Vitro Techniques ; Kinetics ; Male ; Membrane Potentials - drug effects ; nerve terminal impulse ; neuroeffector transmission ; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. 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Increasing the duration of nerve stimulation (100 stimuli at 1 Hz) did not overcome this inhibitory effect. At these concentrations PGE1 and PGE2 were without any apparent inhibitory effect on the amplitudes of spontaneous e.j.ps. 3 Local application of PGE1 (10–100 nM) or PGE2 (10–30 nM) markedly reduced the frequency of occurrence of excitatory junction currents (e.j.cs) evoked by trains of 20–100 stimuli at 1 to 4 Hz without changing the amplitudes of spontaneous e.j.cs or the configuration of the nerve terminal impulse. 4 In the presence of PGE1 or PGE2, raising the frequency of stimulation (from 1 to 4 Hz), increased the likelihood of e.j.c. occurrence. 5 The postjunctional electrical activity recorded in the guinea‐pig vas deferens is believed to be due to ATP released from the sympathetic nerve endings. Thus the present study demonstrates that both PGE1 and PGE2 powerfully inhibit quantal ATP release in the guinea‐pig vas deferens.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Alprostadil - pharmacology</subject><subject>Animals</subject><subject>ATP</subject><subject>Biological and medical sciences</subject><subject>Dinoprostone - pharmacology</subject><subject>electrophysiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>In Vitro Techniques</subject><subject>Kinetics</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>nerve terminal impulse</subject><subject>neuroeffector transmission</subject><subject>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</subject><subject>prejunctional inhibition</subject><subject>prostaglandin E1</subject><subject>prostaglandin E2</subject><subject>sympathetic nerve terminals</subject><subject>vas deferens</subject><subject>Vas Deferens - drug effects</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUsFu1DAQtRBVWQqfgGQhxC3BYydxzAEVqoVWqlQOcLacxMl6lbWDnZTm1k_gG_kSHBqtWl88o_f8xvNmEHoLJIV4PuxTyHiR5KyEFIQo0rGCPCt4evcMbY7Qc7QhhPAEoCxfoJch7AmJIM9P0WnJCwqEb9D9ld2ZyozGWexaPEzeWO07U-PRKxsOJoQFqmY8eBdG1fXKNsbiLeAY4C3FMRl3GndTfKj-3v8ZTIdvVcCNbrXXNnyMRKx7XY_eDbs5yvUu6qseh3Fq5lfopFV90K_X-wz9_Lr9cXGZXN98u7r4fJ0MLH46gSxTTZOVjKmq0ZRAbJDWhWKaCdrmLCcaqkxQYJGTUyI0ENWoKuO0yOtKsDP06UF3mKqDbmptY4O9HLw5KD9Lp4x8ilizk527lSCI4GwReL8KePdr0mGU0Zxa99EQ7aYgeUk5g2Ihvnlc6Vhi9Tzi71ZchWhDG32uTTjSGBDBSB5p5w-036bX8xEGIpcdkHu5DFoug5bLDsh1B-Sd_PL98n_I_gFQSamX</recordid><startdate>199606</startdate><enddate>199606</enddate><creator>Brock, James A.</creator><creator>Cunnane, Thomas C.</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199606</creationdate><title>Inhibition of purinergic transmission by prostaglandin E1 and E2 in the guinea‐pig vas deferens: an electrophysiological study</title><author>Brock, James A. ; Cunnane, Thomas C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p3147-144add4833abde2013812c6a3e392f5350e1b492134835209e10adab47265cb93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Alprostadil - pharmacology</topic><topic>Animals</topic><topic>ATP</topic><topic>Biological and medical sciences</topic><topic>Dinoprostone - pharmacology</topic><topic>electrophysiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>In Vitro Techniques</topic><topic>Kinetics</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>nerve terminal impulse</topic><topic>neuroeffector transmission</topic><topic>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</topic><topic>prejunctional inhibition</topic><topic>prostaglandin E1</topic><topic>prostaglandin E2</topic><topic>sympathetic nerve terminals</topic><topic>vas deferens</topic><topic>Vas Deferens - drug effects</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brock, James A.</creatorcontrib><creatorcontrib>Cunnane, Thomas C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brock, James A.</au><au>Cunnane, Thomas C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of purinergic transmission by prostaglandin E1 and E2 in the guinea‐pig vas deferens: an electrophysiological study</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1996-06</date><risdate>1996</risdate><volume>118</volume><issue>3</issue><spage>776</spage><epage>782</epage><pages>776-782</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1 The effects of prostaglandin E1 (PGE1) and E2 (PGE2) on postjunctional electrical activity in the guinea‐pig vas deferens evoked by sympathetic nerve stimulation were investigated using both intracellular and focal extracellular recording techniques in vitro. 2 Bath application of PGE1 (1–100 nM) or PGE2 (0.1–100 nM) concentration‐dependently inhibited the amplitudes of all excitatory junction potentials (e.j.ps) evoked during short trains of stimuli (10 stimuli at 1 Hz). Increasing the duration of nerve stimulation (100 stimuli at 1 Hz) did not overcome this inhibitory effect. At these concentrations PGE1 and PGE2 were without any apparent inhibitory effect on the amplitudes of spontaneous e.j.ps. 3 Local application of PGE1 (10–100 nM) or PGE2 (10–30 nM) markedly reduced the frequency of occurrence of excitatory junction currents (e.j.cs) evoked by trains of 20–100 stimuli at 1 to 4 Hz without changing the amplitudes of spontaneous e.j.cs or the configuration of the nerve terminal impulse. 4 In the presence of PGE1 or PGE2, raising the frequency of stimulation (from 1 to 4 Hz), increased the likelihood of e.j.c. occurrence. 5 The postjunctional electrical activity recorded in the guinea‐pig vas deferens is believed to be due to ATP released from the sympathetic nerve endings. 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subjects Adenosine Triphosphate - metabolism
Alprostadil - pharmacology
Animals
ATP
Biological and medical sciences
Dinoprostone - pharmacology
electrophysiology
Fundamental and applied biological sciences. Psychology
Guinea Pigs
In Vitro Techniques
Kinetics
Male
Membrane Potentials - drug effects
nerve terminal impulse
neuroeffector transmission
Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ
prejunctional inhibition
prostaglandin E1
prostaglandin E2
sympathetic nerve terminals
vas deferens
Vas Deferens - drug effects
Vertebrates: nervous system and sense organs
title Inhibition of purinergic transmission by prostaglandin E1 and E2 in the guinea‐pig vas deferens: an electrophysiological study
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