Electromechanical coupling in human vas deferens: effects of agents that modulate intracellular release of calcium
Summary The effects of ryanodine, cyclopiazonic acid (CPA) and caffeine on electromechanical coupling in human vas deferens were investigated. High [K+]o (120 mM) evoked nifedipine‐sensitive contractions of longitudinal and circular muscle which consisted of initial and secondary components. Exposur...
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| Veröffentlicht in: | Journal of autonomic pharmacology 1998-06, Vol.18 (3), p.157-165 |
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| creator | Amobi, N. I. B. Smith, I. C. H. |
| description | Summary
The effects of ryanodine, cyclopiazonic acid (CPA) and caffeine on electromechanical coupling in human vas deferens were investigated.
High [K+]o (120 mM) evoked nifedipine‐sensitive contractions of longitudinal and circular muscle which consisted of initial and secondary components.
Exposures to ryanodine (≤10 μM) or CPA (≤ 3 μM) induced a change of basal tension, and higher doses (30 μM) induced intermittent rhythmic contractions of both muscle types in the quiescent tissue. In the presence of the drugs, contraction to high [K+]o was preceded by marked rhythmic activity.
In circular muscle, ryanodine (1–30 μM) or CPA (1–30 μM) reduced both components of contractions to high [K+]o. In longitudinal muscle, the drugs enhanced the initial component and prolonged the secondary component. High doses (≥ 10 μM) produced variable effects on the initial component.
Caffeine (20 mM) reliably contracted longitudinal, but not circular muscle. Pre‐exposures to caffeine enhanced both components in the post‐caffeine contractions of circular muscle to high [K+]o. In longitudinal muscle, only the initial component (post‐caffeine) was enhanced.
Contractions evoked in longitudinal muscle by caffeine were not blocked by ryanodine (30 μM) or CPA (30 μM). However, the enhancement of post‐caffeine contractions to high [K+]o was inhibited.
These results show that ryanodine and CPA produced comparable effects on the excitability of longitudinal and circular muscle in the quiescent tissue, but electromechanical coupling was affected differently. The findings suggest that the muscle types utilize different mechanisms to regulate elevations in cytosolic Ca2+ during stimulation.
Electromechanical coupling in both muscle types involves Ca2+ influx via nifedipine‐sensitive voltage‐operated calcium channels and activation of ryanodine‐sensitive calcium‐induced calcium release from the sacroplasmic reticulum (SR). In longitudinal muscle, the SR also buffers increases in cytosolic Ca2+ via a pharmacologically distinct Ca2+ compartment (caffeine releasable but ryanodine/CPA‐insensitive). In circular muscle, the SR (ryanodine/CPA‐sensitive) serves mainly in the regulation of excitability of the quiescent tissue. |
| doi_str_mv | 10.1046/j.1365-2680.1998.1830157.x |
| format | Article |
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The effects of ryanodine, cyclopiazonic acid (CPA) and caffeine on electromechanical coupling in human vas deferens were investigated.
High [K+]o (120 mM) evoked nifedipine‐sensitive contractions of longitudinal and circular muscle which consisted of initial and secondary components.
Exposures to ryanodine (≤10 μM) or CPA (≤ 3 μM) induced a change of basal tension, and higher doses (30 μM) induced intermittent rhythmic contractions of both muscle types in the quiescent tissue. In the presence of the drugs, contraction to high [K+]o was preceded by marked rhythmic activity.
In circular muscle, ryanodine (1–30 μM) or CPA (1–30 μM) reduced both components of contractions to high [K+]o. In longitudinal muscle, the drugs enhanced the initial component and prolonged the secondary component. High doses (≥ 10 μM) produced variable effects on the initial component.
Caffeine (20 mM) reliably contracted longitudinal, but not circular muscle. Pre‐exposures to caffeine enhanced both components in the post‐caffeine contractions of circular muscle to high [K+]o. In longitudinal muscle, only the initial component (post‐caffeine) was enhanced.
Contractions evoked in longitudinal muscle by caffeine were not blocked by ryanodine (30 μM) or CPA (30 μM). However, the enhancement of post‐caffeine contractions to high [K+]o was inhibited.
These results show that ryanodine and CPA produced comparable effects on the excitability of longitudinal and circular muscle in the quiescent tissue, but electromechanical coupling was affected differently. The findings suggest that the muscle types utilize different mechanisms to regulate elevations in cytosolic Ca2+ during stimulation.
Electromechanical coupling in both muscle types involves Ca2+ influx via nifedipine‐sensitive voltage‐operated calcium channels and activation of ryanodine‐sensitive calcium‐induced calcium release from the sacroplasmic reticulum (SR). In longitudinal muscle, the SR also buffers increases in cytosolic Ca2+ via a pharmacologically distinct Ca2+ compartment (caffeine releasable but ryanodine/CPA‐insensitive). In circular muscle, the SR (ryanodine/CPA‐sensitive) serves mainly in the regulation of excitability of the quiescent tissue.</description><identifier>ISSN: 0144-1795</identifier><identifier>EISSN: 1365-2680</identifier><identifier>DOI: 10.1046/j.1365-2680.1998.1830157.x</identifier><identifier>PMID: 9754636</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Caffeine - pharmacology ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium-Transporting ATPases - antagonists & inhibitors ; Enzyme Inhibitors - pharmacology ; Humans ; In Vitro Techniques ; Indoles - pharmacology ; Male ; Muscle Contraction - drug effects ; Nifedipine - pharmacology ; Ryanodine - pharmacology ; Vas Deferens - drug effects ; Vas Deferens - physiology</subject><ispartof>Journal of autonomic pharmacology, 1998-06, Vol.18 (3), p.157-165</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4157-efb12af72585439510416c4620788a47b38411f01fa76773992a7d24d819e6dc3</citedby><cites>FETCH-LOGICAL-c4157-efb12af72585439510416c4620788a47b38411f01fa76773992a7d24d819e6dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2680.1998.1830157.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2680.1998.1830157.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9754636$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amobi, N. I. B.</creatorcontrib><creatorcontrib>Smith, I. C. H.</creatorcontrib><title>Electromechanical coupling in human vas deferens: effects of agents that modulate intracellular release of calcium</title><title>Journal of autonomic pharmacology</title><addtitle>J Auton Pharmacol</addtitle><description>Summary
The effects of ryanodine, cyclopiazonic acid (CPA) and caffeine on electromechanical coupling in human vas deferens were investigated.
High [K+]o (120 mM) evoked nifedipine‐sensitive contractions of longitudinal and circular muscle which consisted of initial and secondary components.
Exposures to ryanodine (≤10 μM) or CPA (≤ 3 μM) induced a change of basal tension, and higher doses (30 μM) induced intermittent rhythmic contractions of both muscle types in the quiescent tissue. In the presence of the drugs, contraction to high [K+]o was preceded by marked rhythmic activity.
In circular muscle, ryanodine (1–30 μM) or CPA (1–30 μM) reduced both components of contractions to high [K+]o. In longitudinal muscle, the drugs enhanced the initial component and prolonged the secondary component. High doses (≥ 10 μM) produced variable effects on the initial component.
Caffeine (20 mM) reliably contracted longitudinal, but not circular muscle. Pre‐exposures to caffeine enhanced both components in the post‐caffeine contractions of circular muscle to high [K+]o. In longitudinal muscle, only the initial component (post‐caffeine) was enhanced.
Contractions evoked in longitudinal muscle by caffeine were not blocked by ryanodine (30 μM) or CPA (30 μM). However, the enhancement of post‐caffeine contractions to high [K+]o was inhibited.
These results show that ryanodine and CPA produced comparable effects on the excitability of longitudinal and circular muscle in the quiescent tissue, but electromechanical coupling was affected differently. The findings suggest that the muscle types utilize different mechanisms to regulate elevations in cytosolic Ca2+ during stimulation.
Electromechanical coupling in both muscle types involves Ca2+ influx via nifedipine‐sensitive voltage‐operated calcium channels and activation of ryanodine‐sensitive calcium‐induced calcium release from the sacroplasmic reticulum (SR). In longitudinal muscle, the SR also buffers increases in cytosolic Ca2+ via a pharmacologically distinct Ca2+ compartment (caffeine releasable but ryanodine/CPA‐insensitive). In circular muscle, the SR (ryanodine/CPA‐sensitive) serves mainly in the regulation of excitability of the quiescent tissue.</description><subject>Caffeine - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium-Transporting ATPases - antagonists & inhibitors</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Indoles - pharmacology</subject><subject>Male</subject><subject>Muscle Contraction - drug effects</subject><subject>Nifedipine - pharmacology</subject><subject>Ryanodine - pharmacology</subject><subject>Vas Deferens - drug effects</subject><subject>Vas Deferens - physiology</subject><issn>0144-1795</issn><issn>1365-2680</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkElv2zAQhYmiQeqk_QkFiB56k8NNXHJzg6wIWgPpdiNoahjL1eKSUuv8-1Kw4XtP5Myb98j5EPpAyZwSIS82c8plWTCpc8MYPaeaE1qq-e4Vmh2l12hGqBAFVaZ8g85S2hBCpGTsFJ0aVQrJ5QzF6wb8EPsW_Np1tXcN9v24beruGdcdXo-t6_Afl3AFASJ06RJDCNmScB-we4Yu34a1G3DbV2PjBsi2IToPTZPLiCM04BJM0znc12P7Fp0E1yR4dzjP0beb669Xd8Xjl9v7q8Vj4UXepYCwoswFxUpdCm7KvDmVXkhGlNZOqBXXgtJAaHBKKsWNYU5VTFSaGpCV5-fo4z53G_vfI6TBtnWa_uU66MdkFddGS6nz4OV-0Mc-pQjBbmPduvhiKbETcLuxE1U7UbUTcHsAbnfZ_P7wyrhqoTpaD4SzfrPX_9YNvPxHsl0slg-LZa7t1MhBxT6oTgPsjkEu_rJScVXaH59v7fen5dNPRoX9xP8B91ShSw</recordid><startdate>199806</startdate><enddate>199806</enddate><creator>Amobi, N. I. B.</creator><creator>Smith, I. C. H.</creator><general>Blackwell Science Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199806</creationdate><title>Electromechanical coupling in human vas deferens: effects of agents that modulate intracellular release of calcium</title><author>Amobi, N. I. B. ; Smith, I. C. H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4157-efb12af72585439510416c4620788a47b38411f01fa76773992a7d24d819e6dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Caffeine - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium-Transporting ATPases - antagonists & inhibitors</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Indoles - pharmacology</topic><topic>Male</topic><topic>Muscle Contraction - drug effects</topic><topic>Nifedipine - pharmacology</topic><topic>Ryanodine - pharmacology</topic><topic>Vas Deferens - drug effects</topic><topic>Vas Deferens - physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Amobi, N. I. B.</creatorcontrib><creatorcontrib>Smith, I. C. H.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of autonomic pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amobi, N. I. B.</au><au>Smith, I. C. H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electromechanical coupling in human vas deferens: effects of agents that modulate intracellular release of calcium</atitle><jtitle>Journal of autonomic pharmacology</jtitle><addtitle>J Auton Pharmacol</addtitle><date>1998-06</date><risdate>1998</risdate><volume>18</volume><issue>3</issue><spage>157</spage><epage>165</epage><pages>157-165</pages><issn>0144-1795</issn><eissn>1365-2680</eissn><abstract>Summary
The effects of ryanodine, cyclopiazonic acid (CPA) and caffeine on electromechanical coupling in human vas deferens were investigated.
High [K+]o (120 mM) evoked nifedipine‐sensitive contractions of longitudinal and circular muscle which consisted of initial and secondary components.
Exposures to ryanodine (≤10 μM) or CPA (≤ 3 μM) induced a change of basal tension, and higher doses (30 μM) induced intermittent rhythmic contractions of both muscle types in the quiescent tissue. In the presence of the drugs, contraction to high [K+]o was preceded by marked rhythmic activity.
In circular muscle, ryanodine (1–30 μM) or CPA (1–30 μM) reduced both components of contractions to high [K+]o. In longitudinal muscle, the drugs enhanced the initial component and prolonged the secondary component. High doses (≥ 10 μM) produced variable effects on the initial component.
Caffeine (20 mM) reliably contracted longitudinal, but not circular muscle. Pre‐exposures to caffeine enhanced both components in the post‐caffeine contractions of circular muscle to high [K+]o. In longitudinal muscle, only the initial component (post‐caffeine) was enhanced.
Contractions evoked in longitudinal muscle by caffeine were not blocked by ryanodine (30 μM) or CPA (30 μM). However, the enhancement of post‐caffeine contractions to high [K+]o was inhibited.
These results show that ryanodine and CPA produced comparable effects on the excitability of longitudinal and circular muscle in the quiescent tissue, but electromechanical coupling was affected differently. The findings suggest that the muscle types utilize different mechanisms to regulate elevations in cytosolic Ca2+ during stimulation.
Electromechanical coupling in both muscle types involves Ca2+ influx via nifedipine‐sensitive voltage‐operated calcium channels and activation of ryanodine‐sensitive calcium‐induced calcium release from the sacroplasmic reticulum (SR). In longitudinal muscle, the SR also buffers increases in cytosolic Ca2+ via a pharmacologically distinct Ca2+ compartment (caffeine releasable but ryanodine/CPA‐insensitive). In circular muscle, the SR (ryanodine/CPA‐sensitive) serves mainly in the regulation of excitability of the quiescent tissue.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>9754636</pmid><doi>10.1046/j.1365-2680.1998.1830157.x</doi><tpages>9</tpages></addata></record> |
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| ispartof | Journal of autonomic pharmacology, 1998-06, Vol.18 (3), p.157-165 |
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| subjects | Caffeine - pharmacology Calcium - metabolism Calcium Channel Blockers - pharmacology Calcium-Transporting ATPases - antagonists & inhibitors Enzyme Inhibitors - pharmacology Humans In Vitro Techniques Indoles - pharmacology Male Muscle Contraction - drug effects Nifedipine - pharmacology Ryanodine - pharmacology Vas Deferens - drug effects Vas Deferens - physiology |
| title | Electromechanical coupling in human vas deferens: effects of agents that modulate intracellular release of calcium |
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