ALTERED MICROVASCULAR RESPONSES OF THE SMALL-INTESTINE TO SEPSIS DURING RENOVASCULAR HYPERTENSION

Renovascular hypertension alters endothelial-dependent mechanisms to a ffect the response of small arterioles in skeletal muscle to sepsis. S mall arteriole responses to sepsis differ between skeletal muscle and small intestine in normotensives. Our study now shows that renovascula r (1K1C) hypertension alters small arteriole responses in the small in testine to Escherichia coli sepsis. Large arterioles (A1, A2) constric ted by 10-20% in the small intestine of both normotensive and hyperten sive rats during both high and low cardiac output sepsis. Small arteri oles (premucosal A3 and preserosal A4) constricted during high cardiac output sepsis in normotensive but not hypertensive rats. Small A3 and A4 arterioles dilated (20-40%) during low cardiac output sepsis in hy pertensives; but only A3 and not A4 arterioles dilated in normotensive s during low cardiac output sepsis. Acetylcholine, which releases endo thelial-derived relaxing factor in skeletal muscle, dilated both premu cosal A3 and preserosal A4 in both normotensive and hypertensive rats. Thus, hypertension alters small arteriole responses to sepsis in both skeletal muscle and small intestine, but apparently by different mech anisms.