Analysis of ET-A and ET-B receptors using an isolated perfused rat lung preparation.
(2004) In Acta Physiologica Scandinavica 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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/124359
- author
- Granström, Bengt LU ; Nilsson, E ; Hultkvist-Bengtsson, U and Edvinsson, Lars LU
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Acta Physiologica Scandinavica
- volume
- 181
- issue
- 2
- pages
- 259 - 264
- publisher
- Wiley-Blackwell
- external identifiers
-
- wos:000221788600012
- pmid:15180799
- scopus:3042606228
- pmid:15180799
- 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)
- alternative location
- 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
- 2016-04-01 16:15:32
- date last changed
- 2024-02-26 15:13:23
@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 Scandinavica}}, title = {{Analysis of ET-A and ET-B receptors using an isolated perfused rat lung preparation.}}, url = {{https://lup.lub.lu.se/search/files/4618214/624047.pdf}}, doi = {{10.1111/j.1365-201X.2004.01275.x}}, volume = {{181}}, year = {{2004}}, }