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(Circulation Research. 1996;78:231-237.)
© 1996 American Heart Association, Inc.

Articles

Intestinal Absorption of Sodium and Nitric OxideDependent Vasodilation Interact to Dominate Resting Vascular Resistance

H. Glenn Bohlen, Julia M. Lash

From the Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis.

Correspondence to Dr Glenn Bohlen, Department of Physiology and Biophysics, Indiana University Medical School, 635 Barnhill Dr, Indianapolis, IN 46202.

Abstract The villi of the small intestine maintain a hypertonic interstitium at all times, and the submucosal glands constantly secrete ions and accompanying water into the lumen. Generation of the 400- to 600-mOsm interstitial fluid in the villus and secretion by glands may require a large expenditure of energy and, consequently, have major effects on intestinal vascular regulation to supply oxygen and nutrients. Blood flow and oxygen consumption were measured in the ileum of anesthetized rats during natural resting conditions with physiological sodium chloride in the bathing fluid and during isosmotic replacement of sodium chloride with mannitol. Microvascular pressures and blood flow were used to determine the changes in resistance of the major arterioles and the terminal vasculature. When mannitol replaced sodium chloride in contact with the villi, intestinal blood flow decreased to 58.6±2.8% of control, and oxygen consumption was 54.2±3.4% of control. Resistance of the major arterioles increased 101.7±9.9%, and that of the terminal vasculature increased 40.4±6.2%. The increased resistance appeared to be caused by suppression of a nitric oxide mechanism. Local application of 10^-4 mol/L N^G-nitro-L-arginine methyl ester caused about the same reduction in flow and increases in regional vascular resistance as during replacement of sodium but did not alter the oxygen consumption. These data indicate that about half of the intestinal metabolic rate during natural resting conditions is devoted to sodium secretion/absorption. Large resistance vessels are dilated to maintain a high blood flow through release of nitric oxide. We propose that dilation of the terminal vasculature in the metabolically active tissues increased flow velocity sufficiently in the major resistance vessels to cause a flow-mediated release of nitric oxide.

Key Words: intestine • blood flow • oxygen use • nitric oxide • sodium • absorption

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