STRUCTURAL ALTERATIONS OF MICROVASCULAR SMOOTH-MUSCLE CELLS IN REDUCED RENAL MASS HYPERTENSION

被引:15
作者
HANSENSMITH, F
GREENE, AS
COWLEY, AW
LOUGEE, L
LOMBARD, JH
机构
[1] MED COLL WISCONSIN, DEPT PHYSIOL,8701 WATERTOWN PLANK RD, MILWAUKEE, WI 53226 USA
[2] OAKLAND UNIV, DEPT BIOL SCI, ROCHESTER, MI 48063 USA
关键词
MICROCIRCULATION; RENOVASCULAR HYPERTENSION; ARTERIOLES; CAPILLARIES; REDUCED RENAL MASS HYPERTENSION; HISTOLOGY; VASCULAR SMOOTH MUSCLE; RAREFACTION;
D O I
10.1161/01.HYP.17.6.902
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Loss of microvessels (anatomic rarefaction) occurs in chronic reduced renal mass (RRM) hypertension and is mediated via structural degeneration of vascular smooth muscle (VSM) and endothelial cells. The purpose of the present study was to determine if structural changes occur in VSM cells of the microvessels that remain in the tissue of rats with chronic RRM hypertension. Samples of cremaster muscles were taken from normotensive control rats and rats with acute (3-7 days) and chronic (14-28 days) RRM hypertension (75% reduction in kidney mass with 4% NaCl loading). The samples were fixed in situ and processed for light and electron microscopy. Ultrastructural morphology of VSM cells in terminal arterioles of control animals was normal. Although VSM morphology in many microvessels of RRM hypertensive rats was also normal, some vessels exhibited structural changes that were not present in arterioles of the normotensive animals. The most striking change was the appearance of more extensive dense bodies anchoring the contractile filaments around the outer membrane of the cells. Extreme vasoconstriction was observed in some arterioles of RRM rats as long as 2 weeks after salt loading. Focal areas of VSM cell proliferation were evident. Many of the changes occurring in RRM were detected as early as 1 week after the onset of hypertension. These observations suggest that renal mass reduction-salt loading hypertension is associated with early structural and functional changes in the VSM cells.
引用
收藏
页码:902 / 908
页数:7
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