Abstract
We have previously reported that, during chronic hypertension, cerebral arterioles undergo hypertrophy of the vessel wall, accompanied by a paradoxical increase in passive distensibility. We have proposed that this increase may be due to a reduction in the proportion of nondistensible (collagen and basement membrane) to the distensible (smooth muscle, elastin and endothelium) components of the vessel wall. We have recently observed in stroke-prone spontaneously hypertensive rats(SHRSP), that an endothelium derived factor, endothelin, may contribute to hypertrophy, but not to increases in passive ditensibility, of cerebral arterioles vessel wall.The goal of this study was to examine wall mass, composition and passive ditensibility of cerebral arterioles in chronic hypertension induced by decreased availability of another endothelium derived factor, nitric oxide (NO).Four weeks old male Sprague-Dawley rats were treated with LG-nitro-L-arginine methyl ester (LNAME; 10 mg /kg/day) in the drinking water. We examined distensibility of maximally dilated cerebral arterioles in 4 months old Sprague-Dawley rats. Arterioles were then fixed at physiological pressure (2.25% gluterladehyde in 0.10 mol/L cacodylate buffer), the arteriolar segment used for distensibility measurements was removed then immerse fixed, rinsed briefly in 0.1 M cacodylate buffer, osmicated and processed routinely for electron microscopy (TEM).
Published Version
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