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Arterial remodeling and plasma volume expansion in caveolin-1 deficient mice.

Albinsson, Sebastian LU ; Shakirova, Yulia LU ; Rippe, Anna LU ; Baumgarten, Maria LU ; Rosengren, Bert-Inge LU ; Rippe, Catarina LU ; Hallmann, Rupert LU ; Hellstrand, Per LU ; Rippe, Bengt LU and Swärd, Karl LU (2007) In American Journal of Physiology: Regulatory, Integrative and Comparative Physiology 293. p.1222-1231
Abstract
Caveolin- 1 ( Cav- 1) is essential for the morphology of membrane caveolae and exerts a negative influence on a number of signaling systems, including nitric oxide ( NO) production and activity of the MAP kinase cascade. In the vascular system, ablation of caveolin- 1 may thus be expected to cause arterial dilatation and increased vessel wall mass ( remodeling). This was tested in Cav- 1 knockout ( KO) mice by a detailed morphometric and functional analysis of mesenteric resistance arteries, shown to lack caveolae. Quantitative morphometry revealed increased media thickness and media- to- lumen ratio in KO. Pressure- induced myogenic tone and flow- induced dilatation were decreased in KO arteries, but both were increased toward wild- type... (More)
Caveolin- 1 ( Cav- 1) is essential for the morphology of membrane caveolae and exerts a negative influence on a number of signaling systems, including nitric oxide ( NO) production and activity of the MAP kinase cascade. In the vascular system, ablation of caveolin- 1 may thus be expected to cause arterial dilatation and increased vessel wall mass ( remodeling). This was tested in Cav- 1 knockout ( KO) mice by a detailed morphometric and functional analysis of mesenteric resistance arteries, shown to lack caveolae. Quantitative morphometry revealed increased media thickness and media- to- lumen ratio in KO. Pressure- induced myogenic tone and flow- induced dilatation were decreased in KO arteries, but both were increased toward wild- type ( WT) levels following NO synthase ( NOS) inhibition. Isometric force recordings following NOS inhibition showed rightward shifts of passive and active length- force relationships in KO, and the force response to alpha 1- adrenergic stimulation was increased. In contrast, media thickness and force response of the aorta were unaltered in KO vs. WT, whereas lumen diameter was increased. Mean arterial blood pressure during isoflurane anesthesia was not different in KO vs. WT, but greater fluctuation in blood pressure over time was noted. Following NOS inhibition, fluctuations disappeared and pressure increased twice as much in KO ( 38 +/- 6%) compared with WT ( 17 +/- 3%). Tracer- dilution experiments showed increased plasma volume in KO. We conclude that NO affects blood pressure more in Cav- 1 KO than in WT mice and that restructuring of resistance vessels and an increased responsiveness to adrenergic stimulation compensate for a decreased tone in Cav- 1 KO mice. (Less)
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type
Contribution to journal
publication status
published
subject
in
American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
volume
293
pages
1222 - 1231
publisher
American Physiological Society
external identifiers
  • wos:000249156000034
  • scopus:34548457220
ISSN
0363-6119
DOI
10.1152/ajpregu.00092.2007
language
English
LU publication?
yes
id
423720e2-908f-4571-89b3-24344961ef46 (old id 540805)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17626133&dopt=Abstract
date added to LUP
2007-12-04 17:28:23
date last changed
2017-11-05 04:29:05
@article{423720e2-908f-4571-89b3-24344961ef46,
  abstract     = {Caveolin- 1 ( Cav- 1) is essential for the morphology of membrane caveolae and exerts a negative influence on a number of signaling systems, including nitric oxide ( NO) production and activity of the MAP kinase cascade. In the vascular system, ablation of caveolin- 1 may thus be expected to cause arterial dilatation and increased vessel wall mass ( remodeling). This was tested in Cav- 1 knockout ( KO) mice by a detailed morphometric and functional analysis of mesenteric resistance arteries, shown to lack caveolae. Quantitative morphometry revealed increased media thickness and media- to- lumen ratio in KO. Pressure- induced myogenic tone and flow- induced dilatation were decreased in KO arteries, but both were increased toward wild- type ( WT) levels following NO synthase ( NOS) inhibition. Isometric force recordings following NOS inhibition showed rightward shifts of passive and active length- force relationships in KO, and the force response to alpha 1- adrenergic stimulation was increased. In contrast, media thickness and force response of the aorta were unaltered in KO vs. WT, whereas lumen diameter was increased. Mean arterial blood pressure during isoflurane anesthesia was not different in KO vs. WT, but greater fluctuation in blood pressure over time was noted. Following NOS inhibition, fluctuations disappeared and pressure increased twice as much in KO ( 38 +/- 6%) compared with WT ( 17 +/- 3%). Tracer- dilution experiments showed increased plasma volume in KO. We conclude that NO affects blood pressure more in Cav- 1 KO than in WT mice and that restructuring of resistance vessels and an increased responsiveness to adrenergic stimulation compensate for a decreased tone in Cav- 1 KO mice.},
  author       = {Albinsson, Sebastian and Shakirova, Yulia and Rippe, Anna and Baumgarten, Maria and Rosengren, Bert-Inge and Rippe, Catarina and Hallmann, Rupert and Hellstrand, Per and Rippe, Bengt and Swärd, Karl},
  issn         = {0363-6119},
  language     = {eng},
  pages        = {1222--1231},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Regulatory, Integrative and Comparative Physiology},
  title        = {Arterial remodeling and plasma volume expansion in caveolin-1 deficient mice.},
  url          = {http://dx.doi.org/10.1152/ajpregu.00092.2007},
  volume       = {293},
  year         = {2007},
}