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:
https://lup.lub.lu.se/record/606623
- author
- Liuba, Petru
LU
; Karnani, Päivi
; Pesonen, Erkki
LU
; Paakkari, Ilari
; Persson, Kenneth
LU
and Forslid, Anders
LU
- organization
- publishing date
- 2007
- 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
- 2016-04-01 15:58:02
- date last changed
- 2022-04-13 11:22:13
@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 > 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.}},
author = {{Liuba, Petru and Karnani, Päivi and Pesonen, Erkki and Paakkari, Ilari and Persson, Kenneth and Forslid, Anders}},
issn = {{1346-9843}},
keywords = {{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}},
doi = {{10.1253/circj.71.1480}},
volume = {{71}},
year = {{2007}},
}