Ultrastructure of hypertensive rat aorta. Increased basement membrane-like material

J R Guyton, D T Dao, K L Lindsay, A A Taylor
1990 Hypertension  
To determine the effect of elevated blood pressure on the infrastructure of rat aorta, hypertension (average mean pressure 163 ±17 mm Hg) was produced by suprarenal aortic coarctation. After 3 weeks, the subendothelium of the hypertensive thoracic aorta showed significantly increased volume measurements for mononuclear leukocytes and basement membrane-like material compared with the sham-operated control group. Focal areas of rarefaction of the subendothelial extracellular material were
more » ... ed with the nearby presence of mononuclear leukocytes. None of these alterations were found in the normotensive abdominal aorta. The tunica media of hypertensive thoracic aorta also contained significantly increased basement membrane-like material. This new finding in an animal hypertension model is the direct result of the quantitative morphological approach employed in this study. In some rats, the partially constricting aortic ligature compromised the right renal artery leading to ischemic atrophy of the right kidney and hyperreninemia in addition to hypertension. In this group, excluded from the previous analysis and evaluated separately, subendothelial thickening and accumulation of basement membrane-like material in the thoracic aorta were greatly increased compared with the control group and other hypertensive rats. This result could not be attributed to an effect of blood pressure alone and might have been caused in part by humoral factors. Basement membrane accumulation appears to be an important early response of the arterial wall to hypertension or other factors in this rat model. (Hypertension 1990;15:56-67) T he effects of hypertension on the arterial wall include infiltration of the intima with mononuclear blood leukocytes, widening of the subendothelial space, and increase in collagen and elastin content of the tunica media. 1 " 10 Of these effects, leukocytic infiltration has been quantified by light microscopy, 6 -8 but only subendothelial widening has been quantified by ultrastructural morphology. 4 Furthermore, no quantitative estimates are available for the fractional contributions of a variety of component structures to widening of the subendothelial space. Within this space may be found mononuclear blood leukocytes, smooth muscle herniae and cysts, basement membrane-like material, and flocculent material possibly representing insudated plasma protein. 1 -8 A recently developed, microcomputerbased technique for locational stereology 1112 has the ability to quantify common and rare arterial intimal
doi:10.1161/01.hyp.15.1.56 pmid:2295514 fatcat:ajvawctgazcdhom4ocxcjyvupq