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Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection.

Liuba, Petru LU ; Karnani, Päivi; Pesonen, Erkki LU ; Paakkari, Ilari; Persson, Kenneth LU and Forslid, Anders LU (2007) In Circulation Journal 71(9). p.1480-1484
Abstract
Background Impaired muscarinic receptor-mediated vasodilation is an important feature of early atherosclerosis. Earlier studies on apolipoprotein E-knockout mice (apoE-KO) mice suggested adverse effects of Chlamydia pneumoniae infection on the endothelial vasomotor responses of aortas to the muscarinic agonist methacholine. Using additional aorta samples the present study investigated the responses to bradykinin. Methods and Results ApoE-KO mice were repeatedly inoculated with either Chlamydia pneumoniae (C. pneumoniae) or saline. At 2, 6, and 10 weeks after the first inoculation, precontracted aorta rings from both groups were exposed to bradykinin in the absence and presence of L-NAME and diclofenac. In noninfected animals, the vasomotor... (More)
Background Impaired muscarinic receptor-mediated vasodilation is an important feature of early atherosclerosis. Earlier studies on apolipoprotein E-knockout mice (apoE-KO) mice suggested adverse effects of Chlamydia pneumoniae infection on the endothelial vasomotor responses of aortas to the muscarinic agonist methacholine. Using additional aorta samples the present study investigated the responses to bradykinin. Methods and Results ApoE-KO mice were repeatedly inoculated with either Chlamydia pneumoniae (C. pneumoniae) or saline. At 2, 6, and 10 weeks after the first inoculation, precontracted aorta rings from both groups were exposed to bradykinin in the absence and presence of L-NAME and diclofenac. In noninfected animals, the vasomotor responses to bradykinin were similar at all timepoints (p > 0.5). Compared with noninfected animals, the responses in infected animals tended to increase through the study period (p < 0.05 at 10 weeks). Although diclofenac and L-NAME had no effect in noninfected mice, they inhibited the responses to bradykinin in infected mice at 6 and, more markedly, 10 weeks (p < 0.05 for both). Conclusion Bradykinin stimulation of aorta endothelium from C. pneumoniae-infected apoE-KO animals appears to activate compensatory kinin receptor-related mechanisms that could involve nitric oxide and vasorelaxing prostanoids. Although the precise molecular mechanisms require further investigation, one could speculate that strategies increasing bradykinin availability might reverse the arterial dysfunction during chronic infectious disease. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
infection, relaxation, bradykinin, endothelium
in
Circulation Journal
volume
71
issue
9
pages
1480 - 1484
publisher
Japanese Circulation Society
external identifiers
  • wos:000249104400025
  • scopus:34548488708
ISSN
1346-9843
DOI
10.1253/circj.71.1480
language
English
LU publication?
yes
id
8793bb0b-94c1-47f1-adcb-3a28b03f33f8 (old id 606623)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17721032&dopt=Abstract
date added to LUP
2007-12-17 09:51:57
date last changed
2017-01-01 06:51:52
@article{8793bb0b-94c1-47f1-adcb-3a28b03f33f8,
  abstract     = {Background Impaired muscarinic receptor-mediated vasodilation is an important feature of early atherosclerosis. Earlier studies on apolipoprotein E-knockout mice (apoE-KO) mice suggested adverse effects of Chlamydia pneumoniae infection on the endothelial vasomotor responses of aortas to the muscarinic agonist methacholine. Using additional aorta samples the present study investigated the responses to bradykinin. Methods and Results ApoE-KO mice were repeatedly inoculated with either Chlamydia pneumoniae (C. pneumoniae) or saline. At 2, 6, and 10 weeks after the first inoculation, precontracted aorta rings from both groups were exposed to bradykinin in the absence and presence of L-NAME and diclofenac. In noninfected animals, the vasomotor responses to bradykinin were similar at all timepoints (p &gt; 0.5). Compared with noninfected animals, the responses in infected animals tended to increase through the study period (p &lt; 0.05 at 10 weeks). Although diclofenac and L-NAME had no effect in noninfected mice, they inhibited the responses to bradykinin in infected mice at 6 and, more markedly, 10 weeks (p &lt; 0.05 for both). Conclusion Bradykinin stimulation of aorta endothelium from C. pneumoniae-infected apoE-KO animals appears to activate compensatory kinin receptor-related mechanisms that could involve nitric oxide and vasorelaxing prostanoids. Although the precise molecular mechanisms require further investigation, one could speculate that strategies increasing bradykinin availability might reverse the arterial dysfunction during chronic infectious disease.},
  author       = {Liuba, Petru and Karnani, Päivi and Pesonen, Erkki and Paakkari, Ilari and Persson, Kenneth and Forslid, Anders},
  issn         = {1346-9843},
  keyword      = {infection,relaxation,bradykinin,endothelium},
  language     = {eng},
  number       = {9},
  pages        = {1480--1484},
  publisher    = {Japanese Circulation Society},
  series       = {Circulation Journal},
  title        = {Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection.},
  url          = {http://dx.doi.org/10.1253/circj.71.1480},
  volume       = {71},
  year         = {2007},
}