Alpha‐1D adrenoceptors are involved in reserpine‐induced supersensitivity of rat tail artery

We examined reserpine‐induced chemical denervation supersensitivity with special reference to alpha‐1 adrenoceptor (AR) subtypes. Chronic treatment with reserpine for 2 weeks depleted noradrenaline in the tail artery and spleen of rats. Noradrenaline in the thoracic aorta was negligible before and a...

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Veröffentlicht in:British journal of pharmacology 2004-06, Vol.142 (4), p.647-656
Hauptverfasser: Taki, Naoyuki, Tanaka, Takashi, Zhang, Li, Suzuki, Fumiko, Israilova, Malika, Taniguchi, Takanobu, Hiraizumi‐Hiraoka, Yasuko, Shinozuka, Kazumasa, Kunitomo, Masaru, Muramatsu, Ikunobu
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container_issue 4
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container_title British journal of pharmacology
container_volume 142
creator Taki, Naoyuki
Tanaka, Takashi
Zhang, Li
Suzuki, Fumiko
Israilova, Malika
Taniguchi, Takanobu
Hiraizumi‐Hiraoka, Yasuko
Shinozuka, Kazumasa
Kunitomo, Masaru
Muramatsu, Ikunobu
description We examined reserpine‐induced chemical denervation supersensitivity with special reference to alpha‐1 adrenoceptor (AR) subtypes. Chronic treatment with reserpine for 2 weeks depleted noradrenaline in the tail artery and spleen of rats. Noradrenaline in the thoracic aorta was negligible before and after reserpine treatment. The treatment with reserpine produced supersensitivity in the contractile responses of the rat tail artery to phenylephrine, 5‐HT and KCl, resulting in leftward shift of concentration–response curves (11.6‐, 2.5‐ and 1.1‐fold at EC50 value, respectively). These results suggest a predominant sensitization of the alpha‐1 AR‐mediated response by reserpine treatment. BMY 7378 at a concentration (30 nM) specific for blocking the alpha‐1D AR subtype, but not KMD‐3213 at a concentration (10 nM) selective for blocking the alpha‐1A AR subtype, inhibited the supersensitivity of the phenylephrine‐induced response in the reserpine‐treated artery. On the other hand, the response to phenylephrine in reserpine‐untreated artery was selectively inhibited by the same concentration of KMD‐3213, but not by BMY 7378. Prazosin, a subtype‐nonselective antagonist, blocked the responses to phenylephrine with the same potency, regardless of reserpine treatment. In the thoracic aorta and spleen, no supersensitivity was produced in the responses to phenylephrine by reserpine treatment. In a tissue segment‐binding study using [3H]‐prazosin, the total density and affinity of alpha‐1 ARs in the rat tail artery were not changed by treatment with reserpine. However, alpha‐1D AR with high affinity for BMY 7378 was significantly detected in reserpine‐treated tail artery, in contrast to untreated artery. Decreases in alpha‐1A AR with high affinity for KMD‐3213 and alpha‐1B AR with low affinities for KMD‐3213 and BMY 7378 were also estimated in reserpine‐treated tail artery. Alpha‐1D AR mRNA in rat tail artery increased to three‐folds by reserpine treatment, whereas the levels of alpha‐1A and 1B mRNAs were not significantly changed. The present results suggest that chronic treatment with reserpine affects the expression of alpha‐1 AR subtypes of rat tail artery and that the induction of alpha‐1D ARs with high affinity for catecholamines is in part associated with reserpine‐induced supersensitivity. British Journal of Pharmacology (2004) 142, 647–656. doi:10.1038/sj.bjp.0705817
doi_str_mv 10.1038/sj.bjp.0705817
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Chronic treatment with reserpine for 2 weeks depleted noradrenaline in the tail artery and spleen of rats. Noradrenaline in the thoracic aorta was negligible before and after reserpine treatment. The treatment with reserpine produced supersensitivity in the contractile responses of the rat tail artery to phenylephrine, 5‐HT and KCl, resulting in leftward shift of concentration–response curves (11.6‐, 2.5‐ and 1.1‐fold at EC50 value, respectively). These results suggest a predominant sensitization of the alpha‐1 AR‐mediated response by reserpine treatment. BMY 7378 at a concentration (30 nM) specific for blocking the alpha‐1D AR subtype, but not KMD‐3213 at a concentration (10 nM) selective for blocking the alpha‐1A AR subtype, inhibited the supersensitivity of the phenylephrine‐induced response in the reserpine‐treated artery. On the other hand, the response to phenylephrine in reserpine‐untreated artery was selectively inhibited by the same concentration of KMD‐3213, but not by BMY 7378. Prazosin, a subtype‐nonselective antagonist, blocked the responses to phenylephrine with the same potency, regardless of reserpine treatment. In the thoracic aorta and spleen, no supersensitivity was produced in the responses to phenylephrine by reserpine treatment. In a tissue segment‐binding study using [3H]‐prazosin, the total density and affinity of alpha‐1 ARs in the rat tail artery were not changed by treatment with reserpine. However, alpha‐1D AR with high affinity for BMY 7378 was significantly detected in reserpine‐treated tail artery, in contrast to untreated artery. Decreases in alpha‐1A AR with high affinity for KMD‐3213 and alpha‐1B AR with low affinities for KMD‐3213 and BMY 7378 were also estimated in reserpine‐treated tail artery. Alpha‐1D AR mRNA in rat tail artery increased to three‐folds by reserpine treatment, whereas the levels of alpha‐1A and 1B mRNAs were not significantly changed. The present results suggest that chronic treatment with reserpine affects the expression of alpha‐1 AR subtypes of rat tail artery and that the induction of alpha‐1D ARs with high affinity for catecholamines is in part associated with reserpine‐induced supersensitivity. 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Drug treatments ; Phenylephrine - pharmacology ; Piperazines - pharmacology ; Potassium Chloride - pharmacology ; Prazosin - pharmacology ; rat tail artery ; Rats ; Rats, Wistar ; Receptors, Adrenergic, alpha-1 - drug effects ; Receptors, Adrenergic, alpha-1 - physiology ; reserpine ; Reserpine - pharmacology ; RNA, Messenger ; Serotonin - pharmacology ; Spleen - chemistry ; Spleen - drug effects ; Supersensitivity ; Tail - blood supply ; Tail - drug effects ; Tail - metabolism ; Time Factors ; Tritium</subject><ispartof>British journal of pharmacology, 2004-06, Vol.142 (4), p.647-656</ispartof><rights>2004 British Pharmacological Society</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 2004</rights><rights>Copyright 2004, Nature Publishing Group 2004 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5533-b455d9ce9f7dc2f93b15e903250ddb6884583d3a2b88bdb26d4deb120d451733</citedby><cites>FETCH-LOGICAL-c5533-b455d9ce9f7dc2f93b15e903250ddb6884583d3a2b88bdb26d4deb120d451733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575040/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575040/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=15939230$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15159276$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taki, Naoyuki</creatorcontrib><creatorcontrib>Tanaka, Takashi</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Suzuki, Fumiko</creatorcontrib><creatorcontrib>Israilova, Malika</creatorcontrib><creatorcontrib>Taniguchi, Takanobu</creatorcontrib><creatorcontrib>Hiraizumi‐Hiraoka, Yasuko</creatorcontrib><creatorcontrib>Shinozuka, Kazumasa</creatorcontrib><creatorcontrib>Kunitomo, Masaru</creatorcontrib><creatorcontrib>Muramatsu, Ikunobu</creatorcontrib><title>Alpha‐1D adrenoceptors are involved in reserpine‐induced supersensitivity of rat tail artery</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>We examined reserpine‐induced chemical denervation supersensitivity with special reference to alpha‐1 adrenoceptor (AR) subtypes. Chronic treatment with reserpine for 2 weeks depleted noradrenaline in the tail artery and spleen of rats. Noradrenaline in the thoracic aorta was negligible before and after reserpine treatment. The treatment with reserpine produced supersensitivity in the contractile responses of the rat tail artery to phenylephrine, 5‐HT and KCl, resulting in leftward shift of concentration–response curves (11.6‐, 2.5‐ and 1.1‐fold at EC50 value, respectively). These results suggest a predominant sensitization of the alpha‐1 AR‐mediated response by reserpine treatment. BMY 7378 at a concentration (30 nM) specific for blocking the alpha‐1D AR subtype, but not KMD‐3213 at a concentration (10 nM) selective for blocking the alpha‐1A AR subtype, inhibited the supersensitivity of the phenylephrine‐induced response in the reserpine‐treated artery. On the other hand, the response to phenylephrine in reserpine‐untreated artery was selectively inhibited by the same concentration of KMD‐3213, but not by BMY 7378. Prazosin, a subtype‐nonselective antagonist, blocked the responses to phenylephrine with the same potency, regardless of reserpine treatment. In the thoracic aorta and spleen, no supersensitivity was produced in the responses to phenylephrine by reserpine treatment. In a tissue segment‐binding study using [3H]‐prazosin, the total density and affinity of alpha‐1 ARs in the rat tail artery were not changed by treatment with reserpine. However, alpha‐1D AR with high affinity for BMY 7378 was significantly detected in reserpine‐treated tail artery, in contrast to untreated artery. Decreases in alpha‐1A AR with high affinity for KMD‐3213 and alpha‐1B AR with low affinities for KMD‐3213 and BMY 7378 were also estimated in reserpine‐treated tail artery. Alpha‐1D AR mRNA in rat tail artery increased to three‐folds by reserpine treatment, whereas the levels of alpha‐1A and 1B mRNAs were not significantly changed. The present results suggest that chronic treatment with reserpine affects the expression of alpha‐1 AR subtypes of rat tail artery and that the induction of alpha‐1D ARs with high affinity for catecholamines is in part associated with reserpine‐induced supersensitivity. British Journal of Pharmacology (2004) 142, 647–656. doi:10.1038/sj.bjp.0705817</description><subject>alpha‐1 adrenoceptor (AR)</subject><subject>Animals</subject><subject>Aorta, Thoracic - chemistry</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Arteries - drug effects</subject><subject>Arteries - metabolism</subject><subject>Biological and medical sciences</subject><subject>chemical denervation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Administration Schedule</subject><subject>Drug Hypersensitivity</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression - genetics</subject><subject>Indoles - administration &amp; dosage</subject><subject>intact tissue segment binding</subject><subject>Japan</subject><subject>Male</subject><subject>Medical sciences</subject><subject>mRNA</subject><subject>Pharmacology. 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Chronic treatment with reserpine for 2 weeks depleted noradrenaline in the tail artery and spleen of rats. Noradrenaline in the thoracic aorta was negligible before and after reserpine treatment. The treatment with reserpine produced supersensitivity in the contractile responses of the rat tail artery to phenylephrine, 5‐HT and KCl, resulting in leftward shift of concentration–response curves (11.6‐, 2.5‐ and 1.1‐fold at EC50 value, respectively). These results suggest a predominant sensitization of the alpha‐1 AR‐mediated response by reserpine treatment. BMY 7378 at a concentration (30 nM) specific for blocking the alpha‐1D AR subtype, but not KMD‐3213 at a concentration (10 nM) selective for blocking the alpha‐1A AR subtype, inhibited the supersensitivity of the phenylephrine‐induced response in the reserpine‐treated artery. On the other hand, the response to phenylephrine in reserpine‐untreated artery was selectively inhibited by the same concentration of KMD‐3213, but not by BMY 7378. Prazosin, a subtype‐nonselective antagonist, blocked the responses to phenylephrine with the same potency, regardless of reserpine treatment. In the thoracic aorta and spleen, no supersensitivity was produced in the responses to phenylephrine by reserpine treatment. In a tissue segment‐binding study using [3H]‐prazosin, the total density and affinity of alpha‐1 ARs in the rat tail artery were not changed by treatment with reserpine. However, alpha‐1D AR with high affinity for BMY 7378 was significantly detected in reserpine‐treated tail artery, in contrast to untreated artery. Decreases in alpha‐1A AR with high affinity for KMD‐3213 and alpha‐1B AR with low affinities for KMD‐3213 and BMY 7378 were also estimated in reserpine‐treated tail artery. Alpha‐1D AR mRNA in rat tail artery increased to three‐folds by reserpine treatment, whereas the levels of alpha‐1A and 1B mRNAs were not significantly changed. The present results suggest that chronic treatment with reserpine affects the expression of alpha‐1 AR subtypes of rat tail artery and that the induction of alpha‐1D ARs with high affinity for catecholamines is in part associated with reserpine‐induced supersensitivity. British Journal of Pharmacology (2004) 142, 647–656. doi:10.1038/sj.bjp.0705817</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15159276</pmid><doi>10.1038/sj.bjp.0705817</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection
subjects alpha‐1 adrenoceptor (AR)
Animals
Aorta, Thoracic - chemistry
Aorta, Thoracic - drug effects
Arteries - drug effects
Arteries - metabolism
Biological and medical sciences
chemical denervation
Dose-Response Relationship, Drug
Drug Administration Schedule
Drug Hypersensitivity
Gene Expression - drug effects
Gene Expression - genetics
Indoles - administration & dosage
intact tissue segment binding
Japan
Male
Medical sciences
mRNA
Pharmacology. Drug treatments
Phenylephrine - pharmacology
Piperazines - pharmacology
Potassium Chloride - pharmacology
Prazosin - pharmacology
rat tail artery
Rats
Rats, Wistar
Receptors, Adrenergic, alpha-1 - drug effects
Receptors, Adrenergic, alpha-1 - physiology
reserpine
Reserpine - pharmacology
RNA, Messenger
Serotonin - pharmacology
Spleen - chemistry
Spleen - drug effects
Supersensitivity
Tail - blood supply
Tail - drug effects
Tail - metabolism
Time Factors
Tritium
title Alpha‐1D adrenoceptors are involved in reserpine‐induced supersensitivity of rat tail artery
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-16T02%3A06%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Alpha%E2%80%901D%20adrenoceptors%20are%20involved%20in%20reserpine%E2%80%90induced%20supersensitivity%20of%20rat%20tail%20artery&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Taki,%20Naoyuki&rft.date=2004-06&rft.volume=142&rft.issue=4&rft.spage=647&rft.epage=656&rft.pages=647-656&rft.issn=0007-1188&rft.eissn=1476-5381&rft.coden=BJPCBM&rft_id=info:doi/10.1038/sj.bjp.0705817&rft_dat=%3Cproquest_pubme%3E984047591%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=217199349&rft_id=info:pmid/15159276&rfr_iscdi=true