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Increased perfusion pressure enhances the expression of endothelin (ETB) and angiotensin II (AT1, AT2) receptors in rat mesenteric artery smooth muscle cells.

Lindstedt, Isak; Xu, Cang-Bao LU ; Zhang, Yaping LU and Edvinsson, Lars LU (2009) In Blood Pressure 18(1). p.78-85
Abstract
In the present study, we hypothesized that changes in perfusion pressure result in altered expression of mRNA and protein encoding for the ETA-, ETB-, AT1- and AT2-receptors in rat mesenteric vessels. Segments of the rat mesenteric artery were cannulated with glass micropipettes, pressurized and luminally perfused in a perfusion chamber. After either exposure to no ("organ culture" (0 mmHg)), normal (85/75 mmHg) or high pressure (160/150 mmHg) at constant flow for 1-17 h, the vessel segments were snap frozen and real-time polymerase chain reaction was performed to quantify the ET- and AT-receptor mRNA content, or immersed in a fixative solution, dehydrated, frozen, cut in a cryostat and immunohistology stained for ET- and AT-receptor... (More)
In the present study, we hypothesized that changes in perfusion pressure result in altered expression of mRNA and protein encoding for the ETA-, ETB-, AT1- and AT2-receptors in rat mesenteric vessels. Segments of the rat mesenteric artery were cannulated with glass micropipettes, pressurized and luminally perfused in a perfusion chamber. After either exposure to no ("organ culture" (0 mmHg)), normal (85/75 mmHg) or high pressure (160/150 mmHg) at constant flow for 1-17 h, the vessel segments were snap frozen and real-time polymerase chain reaction was performed to quantify the ET- and AT-receptor mRNA content, or immersed in a fixative solution, dehydrated, frozen, cut in a cryostat and immunohistology stained for ET- and AT-receptor protein. The mRNA expressions of ETB and of AT2 were significantly enhanced in vessels exposed to high perfusion pressure, compared with normal and no perfusion pressure at 4 h. In concordance, AT1-, AT2- and ETB-receptor proteins were up-regulated at 17 h of high perfusion pressure. In conclusion, the results from our rat perfusion model suggest a more important role of shear stress than pure pressure alone and may serve as a surrogate model for studies designed to investigate hypertension mechanisms. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Blood Pressure
volume
18
issue
1
pages
78 - 85
publisher
Taylor & Francis
external identifiers
  • wos:000265291000013
  • pmid:19353416
  • scopus:67650124133
ISSN
0803-7051
DOI
10.1080/08037050902850184
language
English
LU publication?
yes
id
c7127739-4110-4c6b-8dd7-334ec6c3219a (old id 1392291)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19353416?dopt=Abstract
date added to LUP
2009-05-06 08:33:56
date last changed
2017-01-01 07:31:39
@article{c7127739-4110-4c6b-8dd7-334ec6c3219a,
  abstract     = {In the present study, we hypothesized that changes in perfusion pressure result in altered expression of mRNA and protein encoding for the ETA-, ETB-, AT1- and AT2-receptors in rat mesenteric vessels. Segments of the rat mesenteric artery were cannulated with glass micropipettes, pressurized and luminally perfused in a perfusion chamber. After either exposure to no ("organ culture" (0 mmHg)), normal (85/75 mmHg) or high pressure (160/150 mmHg) at constant flow for 1-17 h, the vessel segments were snap frozen and real-time polymerase chain reaction was performed to quantify the ET- and AT-receptor mRNA content, or immersed in a fixative solution, dehydrated, frozen, cut in a cryostat and immunohistology stained for ET- and AT-receptor protein. The mRNA expressions of ETB and of AT2 were significantly enhanced in vessels exposed to high perfusion pressure, compared with normal and no perfusion pressure at 4 h. In concordance, AT1-, AT2- and ETB-receptor proteins were up-regulated at 17 h of high perfusion pressure. In conclusion, the results from our rat perfusion model suggest a more important role of shear stress than pure pressure alone and may serve as a surrogate model for studies designed to investigate hypertension mechanisms.},
  author       = {Lindstedt, Isak and Xu, Cang-Bao and Zhang, Yaping and Edvinsson, Lars},
  issn         = {0803-7051},
  language     = {eng},
  number       = {1},
  pages        = {78--85},
  publisher    = {Taylor & Francis},
  series       = {Blood Pressure},
  title        = {Increased perfusion pressure enhances the expression of endothelin (ETB) and angiotensin II (AT1, AT2) receptors in rat mesenteric artery smooth muscle cells.},
  url          = {http://dx.doi.org/10.1080/08037050902850184},
  volume       = {18},
  year         = {2009},
}