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
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