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

被引:45
作者
Albinsson, Sebastian
Shakirova, Yulia
Rippe, Anna
Baumgarten, Maria
Rosengren, Bert-Inge
Rippe, Catarina
Hallmann, Rupert
Hellstrand, Per
Rippe, Bengt
Swaerd, Karl
机构
[1] Lund Univ, Dept Expt Med Sci, Biomed Ctr, SE-22184 Lund, Sweden
[2] Univ Lund Hosp, Dept Nephrol, S-22185 Lund, Sweden
[3] Univ Munster, Inst Physiol Chem & Pathobiochem, D-4400 Munster, Germany
关键词
D O I
10.1152/ajpregu.00092.2007
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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.
引用
收藏
页码:R1222 / R1231
页数:10
相关论文
共 34 条
[1]   Caveolin-1 abolishment attenuates the myogenic response in murine cerebral arteries. (vol 292, pg H1584, 2007) [J].
Adebiyi, A. ;
Zhao, G. ;
Cheranov, S. Y. ;
Ahmed, A. ;
Jaggar, J. H. .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2007, 292 (05) :H2556-H2557
[2]   Cholesterol depletion impairs vascular reactivity to endothelin-1 by reducing store-operated Ca2+ entry dependent on TRPC1 [J].
Bergdahl, A ;
Gomez, MF ;
Dreja, K ;
Xu, SZ ;
Adner, M ;
Beech, DJ ;
Broman, J ;
Hellstrand, P ;
Swärd, K .
CIRCULATION RESEARCH, 2003, 93 (09) :839-847
[3]   An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice [J].
Brandes, RP ;
Schmitz-Winnenthal, FH ;
Félétou, M ;
Gödecke, A ;
Huang, PL ;
Vanhoutte, PM ;
Fleming, I ;
Busse, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (17) :9747-9752
[4]   Role of caveolae and caveolins in health and disease [J].
Cohen, AW ;
Hnasko, R ;
Schubert, W ;
Lisanti, MP .
PHYSIOLOGICAL REVIEWS, 2004, 84 (04) :1341-1379
[5]   Loss of caveolae, vascular dysfunction, and pulmonary defects in caveolin-1 gene-disrupted mice [J].
Drab, M ;
Verkade, P ;
Elger, M ;
Kasper, M ;
Lohn, M ;
Lauterbach, B ;
Menne, J ;
Lindschau, C ;
Mende, F ;
Luft, FC ;
Schedl, A ;
Haller, H ;
Kurzchalia, TV .
SCIENCE, 2001, 293 (5539) :2449-2452
[6]   Cholesterol depletion disrupts caveolae and differentially impairs agonist-induced arterial contraction [J].
Dreja, K ;
Voldstedlund, M ;
Vinten, J ;
Tranum-Jensen, J ;
Hellstrand, P ;
Swärd, K .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (08) :1267-1272
[7]   RETRACTED: RhoA activation and interaction with Caveolin-1 are critical for pressure-induced myogenic tone in rat mesenteric resistance arteries (Publication with Expression of Concern. See vol. 117, pg. 2215, 2021) (Retracted Article) [J].
Dubroca, Caroline ;
Loyer, Xavier ;
Retailleau, Kevin ;
Loirand, Gervalse ;
Pacaud, Pierre ;
Feron, Olivier ;
Balligand, Jean-Luc ;
Levy, Bernard I. ;
Heymes, Christophe ;
Henrion, Daniel .
CARDIOVASCULAR RESEARCH, 2007, 73 (01) :190-197
[8]   PHYSIOLOGICAL-ASPECTS OF PRIMARY HYPERTENSION [J].
FOLKOW, B .
PHYSIOLOGICAL REVIEWS, 1982, 62 (02) :347-504
[9]   Accumulation of molecules involved in α1-adrenergic signal within caveolae:: caveolin expression and the development of cardiac hypertrophy [J].
Fujita, T ;
Toya, Y ;
Iwatsubo, K ;
Onda, T ;
Kimura, K ;
Umemura, S ;
Ishikawa, Y .
CARDIOVASCULAR RESEARCH, 2001, 51 (04) :709-716
[10]   Caveolin-1 expression negatively regulates cell cycle progression by inducing G0/G1 arrest via a p53/p21WAF1/Cip1-dependent mechanism [J].
Galbiati, F ;
Volonte, D ;
Liu, J ;
Capozza, F ;
Frank, PG ;
Zhu, L ;
Pestell, RG ;
Lisanti, MP .
MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (08) :2229-2244