MORPHOLOGY AND FUNCTION OF MESENTERIC RESISTANCE ARTERIES IN TRANSGENIC RATS WITH LOW-RENIN HYPERTENSION

被引:38
作者
THYBO, NK
KORSGAARD, N
MULVANY, MJ
机构
[1] AARHUS UNIV, DEPT PHARMACOL, UNIV PK 240, DK-8000 AARHUS, DENMARK
[2] AARHUS UNIV, DANISH BIOMEMBRANE RES CTR, DK-8000 AARHUS, DENMARK
关键词
TRANSGENIC RATS; SPONTANEOUSLY HYPERTENSIVE RAT; RESISTANCE VESSELS; MORPHOLOGY; MEDIA GROWTH; FUNCTION;
D O I
10.1097/00004872-199210000-00012
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Objective: The renin-angiotensin system plays an important role in blood pressure control. Recently the mouse Ren-2 renin gene was introduced into the genome of rats, producing low-renin hypertensive animals. The aim of the present study was to characterize the pharmacological and morphological properties of mesenteric resistance arteries from transgenic rats. Design: Segments of small arteries were taken from the mesenteric bed of 13-week-old transgenic rats and from age-matched Sprague-Dawley controls. Methods: Vessels were mounted on an isometric myograph permitting direct measurements of vessel isometric wall tension. Vessel morphology was measured with a microscope using a water-immersion objective. Results: The transgenic versus Sprague-Dawley rat comparison is similar to that seen previously for spontaneous hypertensive rats (SHR) versus Wistar-Kyoto (WKY) rats as regards active effective pressure (increased), lumen diameter (decreased) and media thickness (increased). However, in contrast to SHR vessels, where media cross-sectional area has previously been shown to be increased compared with WKY vessels, vessels from transgenic rats had the same media cross-sectional area as those from Sprague-Dawley rats. There was neither cellular hypertrophy nor hyperplasia. However, an increased number of smooth muscle layers was found, indicating a rearrangement of existing material. Conclusion: Although the structural changes found in transgenic rats may account for the increased pressure response, hypertension in this animal is apparently not caused by general vascular growth.
引用
收藏
页码:1191 / 1196
页数:6
相关论文
共 26 条
[1]   EVIDENCE FOR INCREASED MEDIA THICKNESS, INCREASED NEURONAL AMINE UPTAKE, AND DEPRESSED EXCITATION CONTRACTION COUPLING IN ISOLATED RESISTANCE VESSELS FROM ESSENTIAL HYPERTENSIVES [J].
AALKJAER, C ;
HEAGERTY, AM ;
PETERSEN, KK ;
SWALES, JD ;
MULVANY, MJ .
CIRCULATION RESEARCH, 1987, 61 (02) :181-186
[2]   REMODELING OF CEREBRAL ARTERIOLES IN CHRONIC HYPERTENSION [J].
BAUMBACH, GL ;
HEISTAD, DD .
HYPERTENSION, 1989, 13 (06) :968-972
[3]   COMPARISON OF MICROVASCULAR PRESSURES IN NORMAL AND SPONTANEOUSLY HYPERTENSIVE RATS [J].
BOHLEN, HG ;
GORE, RW ;
HUTCHINS, PM .
MICROVASCULAR RESEARCH, 1977, 13 (01) :125-130
[4]   DNA-SYNTHESIS IN ISOLATED ARTERIES - KINETICS AND STRUCTURAL CONSEQUENCES [J].
BOONEN, HCM ;
SCHIFFERS, PMH ;
FAZZI, GE ;
JANSSEN, GMJ ;
DAEMEN, MJAP ;
DEMEY, JGR .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (01) :H210-H217
[5]  
CAMPBELL DJ, 1980, J CLIN INVEST, V79, P1
[6]  
CHRISTENSEN KL, 1989, J HYPERTENS, V7, P83
[7]  
DEMEY JGR, 1991, BASIC RES CARDIOL, V86, P13
[8]   EVIDENCE OF RENIN RELEASE OR PRODUCTION IN SPLANCHNIC TERRITORY [J].
GANTEN, D ;
HAYDUK, K ;
BRECHT, HM ;
BOUCHER, R ;
GENEST, J .
NATURE, 1970, 226 (5245) :551-&
[9]   ANGIOTENSIN-II INDUCES HYPERTROPHY, NOT HYPERPLASIA, OF CULTURED RAT AORTIC SMOOTH-MUSCLE CELLS [J].
GEISTERFER, AAT ;
PEACH, MJ ;
OWENS, GK .
CIRCULATION RESEARCH, 1988, 62 (04) :749-756
[10]  
JUHL CO, 1988, CLIN SCI, V77, P205