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Article: Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles

TitleIntercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles
Authors
Issue Date2007
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajprenal.physiology.org/
Citation
American Journal Of Physiology - Renal Physiology, 2007, v. 292 n. 4, p. F1124-F1131 How to Cite?
AbstractVasoconstriction and increase in the intracellular calcium concentration ([Ca2+]i) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca2+]i, which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2′,7′- difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-L-arginine methyl ester (L-NAME). Depolarization increased smooth muscle cell [Ca2+] i from 162 ± 15 nmol/l to a peak of 555 ± 70 nmol/l (n = 7), and this response was inhibited by 80% by the L-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca2+]i increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 μm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO]i) which was inhibited by L-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca2+]i, which did not transfer to the smooth muscle cells. L-NAME treatment did not affect changes in smooth muscle [Ca 2+]i after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca2+]i which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/80255
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorUhrenholt, TRen_HK
dc.contributor.authorSchjerning, Jen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorJensen, BLen_HK
dc.contributor.authorSkøtt, Oen_HK
dc.date.accessioned2010-09-06T08:04:16Z-
dc.date.available2010-09-06T08:04:16Z-
dc.date.issued2007en_HK
dc.identifier.citationAmerican Journal Of Physiology - Renal Physiology, 2007, v. 292 n. 4, p. F1124-F1131en_HK
dc.identifier.issn0363-6127en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80255-
dc.description.abstractVasoconstriction and increase in the intracellular calcium concentration ([Ca2+]i) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca2+]i, which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2′,7′- difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-L-arginine methyl ester (L-NAME). Depolarization increased smooth muscle cell [Ca2+] i from 162 ± 15 nmol/l to a peak of 555 ± 70 nmol/l (n = 7), and this response was inhibited by 80% by the L-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca2+]i increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 μm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO]i) which was inhibited by L-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca2+]i, which did not transfer to the smooth muscle cells. L-NAME treatment did not affect changes in smooth muscle [Ca 2+]i after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca2+]i which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus. Copyright © 2007 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajprenal.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiologyen_HK
dc.subject.meshAcetylcholine - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshArterioles - physiologyen_HK
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCalcium Signaling - drug effects - physiologyen_HK
dc.subject.meshEndothelial Cells - drug effects - physiologyen_HK
dc.subject.meshFeedbacken_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicroscopy, Fluorescenceen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNitric Oxide - pharmacologyen_HK
dc.subject.meshPerfusionen_HK
dc.subject.meshPotassium Chloride - pharmacologyen_HK
dc.subject.meshRabbitsen_HK
dc.subject.meshVasoconstriction - drug effects - physiologyen_HK
dc.titleIntercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arteriolesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1931-857X&volume=292&spage=1124&epage=1131&date=2007&atitle=Intercellular+calcium+signaling+and+nitric+oxide+feedback+during+constriction+of+rabbit+renal+afferent+arteriolesen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajprenal.00420.2006en_HK
dc.identifier.pmid17148782-
dc.identifier.scopuseid_2-s2.0-34147098604en_HK
dc.identifier.hkuros136343en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34147098604&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume292en_HK
dc.identifier.issue4en_HK
dc.identifier.spageF1124en_HK
dc.identifier.epageF1131en_HK
dc.identifier.isiWOS:000245469200002-
dc.identifier.f10001100089-
dc.identifier.scopusauthoridUhrenholt, TR=6506710961en_HK
dc.identifier.scopusauthoridSchjerning, J=6507253589en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridJensen, BL=35502338900en_HK
dc.identifier.scopusauthoridSkøtt, O=7005724990en_HK

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