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Analysis of ET-A and ET-B receptors using an isolated perfused rat lung preparation.

Granström, Bengt LU ; Nilsson, E; Hultkvist-Bengtsson, U and Edvinsson, Lars LU (2004) In Acta Physiologica Scandinavica1888-12-31+01:002006-01-01+01:00 181(2). p.259-264
Abstract
Aims and Methods: The pulmonary and vascular effects of endothelin-1 receptor activation were studied in isolated perfused and ventilated lung preparations from rat. The responses to endothelin-1 (ET-1) and the endothelin B (ETB) receptor agonist sarafotoxin 6c (S6c) were characterized using the endothelin A (ETA)-receptor antagonist FR 139317, the ETB-receptor antagonist BQ 788 and the combined ETA/ETB-receptor antagonist Bosentan. The respiratory parameter airway conductance (Gaw) and the vascular parameter perfusion flow were analysed simultaneously.



Results: Concentration-response curves for ET-1 administered intra-arterially revealed that its most potent effect was on the vascular side while S6c had a more potent... (More)
Aims and Methods: The pulmonary and vascular effects of endothelin-1 receptor activation were studied in isolated perfused and ventilated lung preparations from rat. The responses to endothelin-1 (ET-1) and the endothelin B (ETB) receptor agonist sarafotoxin 6c (S6c) were characterized using the endothelin A (ETA)-receptor antagonist FR 139317, the ETB-receptor antagonist BQ 788 and the combined ETA/ETB-receptor antagonist Bosentan. The respiratory parameter airway conductance (Gaw) and the vascular parameter perfusion flow were analysed simultaneously.



Results: Concentration-response curves for ET-1 administered intra-arterially revealed that its most potent effect was on the vascular side while S6c had a more potent effect on airway conductance. ET-1, given as a bolus dose intra-arterially (100 muL of 0.2 nm), induced a strong- and long-lasting contraction of the vasculature while only a less pronounced contraction was seen in the airways. Neither of the antagonists had a significant effect per se on Gaw or perfusion flow. FR 139317 reduced the effect of ET-1 on perfusion flow by about 50%, while airway conductance was augmented. BQ 788 enhanced the decrease in perfusion flow by ET-1 while Gaw was not influenced. The combined ETA/ETB antagonist Bosentan powerfully prevented the ET-1-induced decrease in Gaw but did not alter its reduction in perfusion flow.



Conclusions: The potent effect of ET-1 on the vascular side of the lung is mediated mainly through ETA receptors, whereas both ETA and ETB receptors are involved in Gaw in the rat lung. (Less)
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Contribution to journal
publication status
published
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in
Acta Physiologica Scandinavica1888-12-31+01:002006-01-01+01:00
volume
181
issue
2
pages
259 - 264
publisher
Wiley-Blackwell
external identifiers
  • wos:000221788600012
  • pmid:15180799
  • scopus:3042606228
ISSN
0001-6772
DOI
10.1111/j.1365-201X.2004.01275.x
language
English
LU publication?
yes
id
656bba83-791f-4357-9283-bf9c1b8987ec (old id 124359)
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http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15180799&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
date added to LUP
2007-06-29 08:55:12
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2017-11-27 13:21:32
@article{656bba83-791f-4357-9283-bf9c1b8987ec,
  abstract     = {Aims and Methods: The pulmonary and vascular effects of endothelin-1 receptor activation were studied in isolated perfused and ventilated lung preparations from rat. The responses to endothelin-1 (ET-1) and the endothelin B (ETB) receptor agonist sarafotoxin 6c (S6c) were characterized using the endothelin A (ETA)-receptor antagonist FR 139317, the ETB-receptor antagonist BQ 788 and the combined ETA/ETB-receptor antagonist Bosentan. The respiratory parameter airway conductance (Gaw) and the vascular parameter perfusion flow were analysed simultaneously.<br/><br>
<br/><br>
Results: Concentration-response curves for ET-1 administered intra-arterially revealed that its most potent effect was on the vascular side while S6c had a more potent effect on airway conductance. ET-1, given as a bolus dose intra-arterially (100 muL of 0.2 nm), induced a strong- and long-lasting contraction of the vasculature while only a less pronounced contraction was seen in the airways. Neither of the antagonists had a significant effect per se on Gaw or perfusion flow. FR 139317 reduced the effect of ET-1 on perfusion flow by about 50%, while airway conductance was augmented. BQ 788 enhanced the decrease in perfusion flow by ET-1 while Gaw was not influenced. The combined ETA/ETB antagonist Bosentan powerfully prevented the ET-1-induced decrease in Gaw but did not alter its reduction in perfusion flow.<br/><br>
<br/><br>
Conclusions: The potent effect of ET-1 on the vascular side of the lung is mediated mainly through ETA receptors, whereas both ETA and ETB receptors are involved in Gaw in the rat lung.},
  author       = {Granström, Bengt and Nilsson, E and Hultkvist-Bengtsson, U and Edvinsson, Lars},
  issn         = {0001-6772},
  language     = {eng},
  number       = {2},
  pages        = {259--264},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Physiologica Scandinavica1888-12-31+01:002006-01-01+01:00},
  title        = {Analysis of ET-A and ET-B receptors using an isolated perfused rat lung preparation.},
  url          = {http://dx.doi.org/10.1111/j.1365-201X.2004.01275.x},
  volume       = {181},
  year         = {2004},
}