Inward remodeling follows chronic vasoconstriction in isolated resistance arteries

被引:118
作者
Bakker, ENTP
van der Meulen, ET
van den Berg, BM
Everts, V
Spaan, JAE
VanBavel, E
机构
[1] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands
[2] Acad Ctr Dent Amsterdam, Dept Cell Biol & Histol, NL-1066 EA Amsterdam, Netherlands
[3] Acad Ctr Dent Amsterdam, Dept Periodontol, NL-1066 EA Amsterdam, Netherlands
[4] Acad Med Ctr, Dept Med Phys, Amsterdam, Netherlands
[5] Acad Med Ctr, Cardiovasc Res Inst Amsterdam, Amsterdam, Netherlands
关键词
rat; resistance arteries; remodeling; vasoconstriction;
D O I
10.1159/000048989
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The hypothesis was tested that chronic vasoconstriction is followed by a structural reduction in lumen diameter, measured at full dilation. An in vitro model of pressurized rat skeletal muscle arterioles was used. During a 3-day experimental period, constriction of active vessels was achieved with fetal calf serum or endothelin-1 (ET-1). Maximal dilation revealed inward remodeling from 179 +/- 6.5 mum lumen diameter on day 0 to 151 +/- 6.3 mum on day 3 at 75 mm Hg in vessels incubated with serum (n = 8). Similarly, ET-1 induced inward remodeling from 182 +/- 5.2 to 164 +/- 3.7 mum (n = 6). When constriction during organoid culture was inhibited with papaverin or verapamil, inward remodeling was fully prevented: 184 +/- 6.3 to 184 +/- 5.8 mum for papaverin (n = 6) and 174 +/- 5.5 to 177 +/- 7.4 mum for verapamil (n = 6). A chronic reduction in diameter without tone was achieved in vessels that were kept at a low pressure (2-5 mm Hg; n = 6). Here, no remodeling was found, thereby ruling out that a chronic reduction in diameter alone is sufficient for inward remodeling. These data show that a persistent active reduction in lumen diameter is followed by inward remodeling of arterioles. Copyright (C) 2002 S. Karger AG, Basel.
引用
收藏
页码:12 / 20
页数:9
相关论文
共 16 条
[1]  
Bakker ENTP, 2000, AM J PHYSIOL-HEART C, V278, pH1233
[2]   Contribution of collagen, elastin, and smooth muscle to in vivo human brachial artery wall stress and elastic modulus [J].
Bank, AJ ;
Wang, HY ;
Holte, JE ;
Mullen, K ;
Shammas, R ;
Kubo, SH .
CIRCULATION, 1996, 94 (12) :3263-3270
[3]   VASOACTIVE EFFECTS OF GROWTH-FACTORS [J].
BERK, BC ;
ALEXANDER, RW .
BIOCHEMICAL PHARMACOLOGY, 1989, 38 (02) :219-225
[4]   Regulation of cardiovascular collagen synthesis by mechanical load [J].
Bishop, JE ;
Lindahl, G .
CARDIOVASCULAR RESEARCH, 1999, 42 (01) :27-44
[5]   Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries [J].
Buus, CL ;
Pourageaud, F ;
Fazzi, GE ;
Janssen, G ;
Mulvany, MJ ;
De Mey, JGR .
CIRCULATION RESEARCH, 2001, 89 (02) :180-186
[6]   Transmural pressure induces matrix-degrading activity in porcine arteries ex vivo [J].
Chesler, NC ;
Ku, DN ;
Galis, ZS .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1999, 277 (05) :H2002-H2009
[7]   ACUTE AND LONG-TERM EFFECTS OF TISSUE-CULTURE ON CONTRACTILE REACTIVITY IN RENAL-ARTERIES OF THE RAT [J].
DEMEY, JGR ;
UITENDAAL, MP ;
BOONEN, HCM ;
VRIJDAG, MJJF ;
DAEMEN, MJAP ;
STRUYKERBOUDIER, HAJ .
CIRCULATION RESEARCH, 1989, 65 (04) :1125-1135
[8]   MECHANICAL-PROPERTIES OF ARTERIES [J].
DOBRIN, PB .
PHYSIOLOGICAL REVIEWS, 1978, 58 (02) :397-460
[9]   CYTOKINE-STIMULATED HUMAN VASCULAR SMOOTH-MUSCLE CELLS SYNTHESIZE A COMPLEMENT OF ENZYMES REQUIRED FOR EXTRACELLULAR-MATRIX DIGESTION [J].
GALIS, ZS ;
MUSZYNSKI, M ;
SUKHOVA, GK ;
SIMONMORRISSEY, E ;
UNEMORI, EN ;
LARK, MW ;
AMENTO, E ;
LIBBY, P .
CIRCULATION RESEARCH, 1994, 75 (01) :181-189
[10]   SMALL ARTERY STRUCTURE IN HYPERTENSION - DUAL PROCESSES OF REMODELING AND GROWTH [J].
HEAGERTY, AM ;
AALKJAER, C ;
BUND, SJ ;
KORSGAARD, N ;
MULVANY, MJ .
HYPERTENSION, 1993, 21 (04) :391-397