Vascular Endothelial σ1-Receptor Stimulation With SA4503 Rescues Aortic Relaxation via Akt/eNOS Signaling in Ovariectomized Rats With Aortic Banding

Background: We previously reported that σ1-receptor (σ1R) expression in the thoracic aorta decreased after pressure overload (PO) induced by abdominal aortic banding in ovariectomized (OVX) rats. Here, we asked whether stimulation of σ1R with the selective agonist SA4503 elicits functional recovery...

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Veröffentlicht in:Circulation Journal 2013, Vol.77(11), pp.2831-2840
Hauptverfasser: Tagashira, Hideaki, Matsumoto, Takayuki, Taguchi, Kumiko, Zhang, Chen, Han, Feng, Ishida, Keiko, Nemoto, Shingo, Kobayashi, Tsuneo, Fukunaga, Kohji
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container_end_page 2840
container_issue 11
container_start_page 2831
container_title Circulation Journal
container_volume 77
creator Tagashira, Hideaki
Matsumoto, Takayuki
Taguchi, Kumiko
Zhang, Chen
Han, Feng
Ishida, Keiko
Nemoto, Shingo
Kobayashi, Tsuneo
Fukunaga, Kohji
description Background: We previously reported that σ1-receptor (σ1R) expression in the thoracic aorta decreased after pressure overload (PO) induced by abdominal aortic banding in ovariectomized (OVX) rats. Here, we asked whether stimulation of σ1R with the selective agonist SA4503 elicits functional recovery of aortic vasodilation and constriction following vascular injury in OVX rats with PO. Methods and Results: SA4503 (0.3–1.0mg/kg) and NE-100 (a σ1R antagonist, 1.0mg/kg) were administered orally for 4 weeks (once daily) to OVX-PO rats. Vascular functions of isolated descending aorta were measured following phenylephrine (PE)- or endothelin-1 (ET-1)-induced vasoconstriction and acetylcholine (ACh)- or clonidine-induced vasodilation. SA4503 administration rescued PO-induced σ1R decreases in aortic smooth muscle and endothelial cells. SA4503 treatment also rescued PO-induced impairments in ACh- and clonidine-induced vasodilation without affecting PE- and ET-1-induced vasoconstriction. Ameliorated ACh- and clonidine-induced vasodilation was closely associated with increased Akt activity and in turn endothelial nitric oxide synthase (eNOS) phosphorylation. The SA4503-mediated improvement of vasodilation was blocked by NE-100 treatment. Conclusions: σ1R is downregulated following PO-induced endothelial injury in OVX rats. The selective σ1R agonist SA4503 rescues impaired endothelium-dependent vasodilation in the aorta from OVX-PO rats through σ1R stimulation, enhancing eNOS-cGMP signaling in vascular endothelial cells. These observations encourage development of novel therapeutics targeting σ1R to prevent vascular endothelial injury in vascular diseases.  (Circ J 2013; 77: 2831–2840)
doi_str_mv 10.1253/circj.CJ-13-0256
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Here, we asked whether stimulation of σ1R with the selective agonist SA4503 elicits functional recovery of aortic vasodilation and constriction following vascular injury in OVX rats with PO. Methods and Results: SA4503 (0.3–1.0mg/kg) and NE-100 (a σ1R antagonist, 1.0mg/kg) were administered orally for 4 weeks (once daily) to OVX-PO rats. Vascular functions of isolated descending aorta were measured following phenylephrine (PE)- or endothelin-1 (ET-1)-induced vasoconstriction and acetylcholine (ACh)- or clonidine-induced vasodilation. SA4503 administration rescued PO-induced σ1R decreases in aortic smooth muscle and endothelial cells. SA4503 treatment also rescued PO-induced impairments in ACh- and clonidine-induced vasodilation without affecting PE- and ET-1-induced vasoconstriction. Ameliorated ACh- and clonidine-induced vasodilation was closely associated with increased Akt activity and in turn endothelial nitric oxide synthase (eNOS) phosphorylation. The SA4503-mediated improvement of vasodilation was blocked by NE-100 treatment. Conclusions: σ1R is downregulated following PO-induced endothelial injury in OVX rats. The selective σ1R agonist SA4503 rescues impaired endothelium-dependent vasodilation in the aorta from OVX-PO rats through σ1R stimulation, enhancing eNOS-cGMP signaling in vascular endothelial cells. These observations encourage development of novel therapeutics targeting σ1R to prevent vascular endothelial injury in vascular diseases.  (Circ J 2013; 77: 2831–2840)</description><identifier>ISSN: 1346-9843</identifier><identifier>EISSN: 1347-4820</identifier><identifier>DOI: 10.1253/circj.CJ-13-0256</identifier><identifier>PMID: 23965801</identifier><language>eng</language><publisher>Japan: The Japanese Circulation Society</publisher><subject>Adrenergic alpha-1 Receptor Agonists - pharmacology ; Animals ; Anisoles - pharmacology ; Antipsychotic Agents - pharmacology ; Aorta, Abdominal - injuries ; Aorta, Abdominal - metabolism ; Aorta, Abdominal - pathology ; Aortic Diseases - metabolism ; Aortic Diseases - pathology ; Cyclic GMP - metabolism ; Endothelial nitric oxide synthase ; Endothelin-1 - pharmacology ; Endothelium, Vascular - injuries ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Female ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Nitric Oxide Synthase Type III - metabolism ; Nootropic Agents - pharmacology ; Ovariectomy ; Phenylephrine - pharmacology ; Phosphorylation - drug effects ; Piperazines - pharmacology ; Propylamines - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Rats, Wistar ; Receptors, sigma - agonists ; Receptors, sigma - metabolism ; Sigma-1 Receptor ; Vascular disease ; Vasodilation - drug effects ; σ1-receptor</subject><ispartof>Circulation Journal, 2013, Vol.77(11), pp.2831-2840</ispartof><rights>2013 THE JAPANESE CIRCULATION SOCIETY</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-35564576c0add05b6d5839d6001c96a231201db368b14a8b608cf488af1ba3a53</citedby><cites>FETCH-LOGICAL-c434t-35564576c0add05b6d5839d6001c96a231201db368b14a8b608cf488af1ba3a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23965801$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tagashira, Hideaki</creatorcontrib><creatorcontrib>Matsumoto, Takayuki</creatorcontrib><creatorcontrib>Taguchi, Kumiko</creatorcontrib><creatorcontrib>Zhang, Chen</creatorcontrib><creatorcontrib>Han, Feng</creatorcontrib><creatorcontrib>Ishida, Keiko</creatorcontrib><creatorcontrib>Nemoto, Shingo</creatorcontrib><creatorcontrib>Kobayashi, Tsuneo</creatorcontrib><creatorcontrib>Fukunaga, Kohji</creatorcontrib><title>Vascular Endothelial σ1-Receptor Stimulation With SA4503 Rescues Aortic Relaxation via Akt/eNOS Signaling in Ovariectomized Rats With Aortic Banding</title><title>Circulation Journal</title><addtitle>Circ J</addtitle><description>Background: We previously reported that σ1-receptor (σ1R) expression in the thoracic aorta decreased after pressure overload (PO) induced by abdominal aortic banding in ovariectomized (OVX) rats. Here, we asked whether stimulation of σ1R with the selective agonist SA4503 elicits functional recovery of aortic vasodilation and constriction following vascular injury in OVX rats with PO. Methods and Results: SA4503 (0.3–1.0mg/kg) and NE-100 (a σ1R antagonist, 1.0mg/kg) were administered orally for 4 weeks (once daily) to OVX-PO rats. Vascular functions of isolated descending aorta were measured following phenylephrine (PE)- or endothelin-1 (ET-1)-induced vasoconstriction and acetylcholine (ACh)- or clonidine-induced vasodilation. SA4503 administration rescued PO-induced σ1R decreases in aortic smooth muscle and endothelial cells. SA4503 treatment also rescued PO-induced impairments in ACh- and clonidine-induced vasodilation without affecting PE- and ET-1-induced vasoconstriction. Ameliorated ACh- and clonidine-induced vasodilation was closely associated with increased Akt activity and in turn endothelial nitric oxide synthase (eNOS) phosphorylation. The SA4503-mediated improvement of vasodilation was blocked by NE-100 treatment. Conclusions: σ1R is downregulated following PO-induced endothelial injury in OVX rats. The selective σ1R agonist SA4503 rescues impaired endothelium-dependent vasodilation in the aorta from OVX-PO rats through σ1R stimulation, enhancing eNOS-cGMP signaling in vascular endothelial cells. 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Here, we asked whether stimulation of σ1R with the selective agonist SA4503 elicits functional recovery of aortic vasodilation and constriction following vascular injury in OVX rats with PO. Methods and Results: SA4503 (0.3–1.0mg/kg) and NE-100 (a σ1R antagonist, 1.0mg/kg) were administered orally for 4 weeks (once daily) to OVX-PO rats. Vascular functions of isolated descending aorta were measured following phenylephrine (PE)- or endothelin-1 (ET-1)-induced vasoconstriction and acetylcholine (ACh)- or clonidine-induced vasodilation. SA4503 administration rescued PO-induced σ1R decreases in aortic smooth muscle and endothelial cells. SA4503 treatment also rescued PO-induced impairments in ACh- and clonidine-induced vasodilation without affecting PE- and ET-1-induced vasoconstriction. Ameliorated ACh- and clonidine-induced vasodilation was closely associated with increased Akt activity and in turn endothelial nitric oxide synthase (eNOS) phosphorylation. The SA4503-mediated improvement of vasodilation was blocked by NE-100 treatment. Conclusions: σ1R is downregulated following PO-induced endothelial injury in OVX rats. The selective σ1R agonist SA4503 rescues impaired endothelium-dependent vasodilation in the aorta from OVX-PO rats through σ1R stimulation, enhancing eNOS-cGMP signaling in vascular endothelial cells. These observations encourage development of novel therapeutics targeting σ1R to prevent vascular endothelial injury in vascular diseases.  (Circ J 2013; 77: 2831–2840)</abstract><cop>Japan</cop><pub>The Japanese Circulation Society</pub><pmid>23965801</pmid><doi>10.1253/circj.CJ-13-0256</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Adrenergic alpha-1 Receptor Agonists - pharmacology
Animals
Anisoles - pharmacology
Antipsychotic Agents - pharmacology
Aorta, Abdominal - injuries
Aorta, Abdominal - metabolism
Aorta, Abdominal - pathology
Aortic Diseases - metabolism
Aortic Diseases - pathology
Cyclic GMP - metabolism
Endothelial nitric oxide synthase
Endothelin-1 - pharmacology
Endothelium, Vascular - injuries
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Female
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
Nitric Oxide Synthase Type III - metabolism
Nootropic Agents - pharmacology
Ovariectomy
Phenylephrine - pharmacology
Phosphorylation - drug effects
Piperazines - pharmacology
Propylamines - pharmacology
Proto-Oncogene Proteins c-akt - metabolism
Rats, Wistar
Receptors, sigma - agonists
Receptors, sigma - metabolism
Sigma-1 Receptor
Vascular disease
Vasodilation - drug effects
σ1-receptor
title Vascular Endothelial σ1-Receptor Stimulation With SA4503 Rescues Aortic Relaxation via Akt/eNOS Signaling in Ovariectomized Rats With Aortic Banding
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