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  • Nilsson, DavidLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine (författare)

Endothelin receptor-mediated vasodilatation: Effects of organ culture.

  • Artikel/kapitelEngelska2008

Förlag, utgivningsår, omfång ...

  • Elsevier BV,2008

Nummerbeteckningar

  • LIBRIS-ID:oai:lup.lub.lu.se:49da8ed9-133a-479b-a8b2-93521f6b9240
  • https://lup.lub.lu.se/record/608266URI
  • https://doi.org/10.1016/j.ejphar.2007.09.031DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:art swepub-publicationtype
  • Ämneskategori:ref swepub-contenttype

Anmärkningar

  • Culture of intact arteries is a frequently employed experimental model for investigating the mechanisms governing the regulation of vascular endothelin receptors. Endothelin type A (ETA) and type B (ETB) receptors on vascular smooth muscle cells are up-regulated in organ culture and the enhanced vasoconstriction mimics the changes that occur in cardiovascular disease. The effect of organ culture on endothelial dilatory endothelin ETB receptors is not known. We hypothesize that organ culture decreases the endothelin receptor-mediated dilatation and that this is one possible mechanism by which the effects of the endothelin in blood vessels are altered during culture. Porcine coronary arteries were studied before and after 24 h of culture, using in vitro pharmacology and immunofluorescence. Sarafotoxin 6c and endothelin-1 were used to examine the endothelin ETA and ETB receptor effects, and the antagonists, Nω-nitro-l-arginine (l-NOARG) for nitric oxide (NO), indomethacin for prostaglandins and charybdotoxin in combination with apamin for endothelium-derived hyperpolarizing factor (EDHF), were used to study the endothelium-derived dilatory mediators. Organ culture induced up-regulation of the sarafotoxin 6c (ETB receptor agonist) and endothelin-1 (ETA receptor agonist) elicited vasoconstriction. The sarafotoxin 6c contraction was stronger after endothelium denudation, suggesting endothelium-dependent dilatation. The endothelin-1 contraction was not affected by endothelium denudation. The increase in sarafotoxin 6c contraction after removal of the endothelium was more pronounced before than after organ culture, suggesting down-regulated endothelial endothelin ETB receptors. Also, the immunofluorescence staining intensities for endothelial endothelin ETB receptors were higher before than after organ culture. Pre-incubation with inhibitors for dilatory mediators suggested that both NO and EDHF play a vasodilatory role, while prostaglandins are not involved. In conclusion, endothelial endothelin ETB receptors induce NO and EDHF mediated vasodilatation in porcine coronary arteries. In organ culture, endothelial endothelin ETB receptors are down-regulated, mimicking the changes that occur in cardiovascular disease. Down-regulation of endothelial endothelin ETB receptors may in part explain the increased endothelin ETB receptor-mediated vasoconstriction frequently studied in organ culture.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Wackenfors, AngelicaLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)med-awa (författare)
  • Gustafsson, LottaLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund(Swepub:lu)fysi-lgu (författare)
  • Ugander, MartinLund University,Lunds universitet,Klinisk fysiologi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Clinical Physiology (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)klfy-mug (författare)
  • Paulsson, PerLund University,Lunds universitet,Thoraxkirurgi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Thoracic Surgery,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)thor-ppa (författare)
  • Ingemansson, RichardLund University,Lunds universitet,Thoraxkirurgi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Thoracic Surgery,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)thor-rin (författare)
  • Edvinsson, LarsLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)med-led (författare)
  • Malmsjö, MalinLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund(Swepub:lu)med-mma (författare)
  • Medicin, LundSektion II (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:European Journal of Pharmacology: Elsevier BV579:1-3, s. 233-2401879-07120014-2999

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