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.
| Original language | English |
|---|---|
| Pages (from-to) | 231-237 |
| Number of pages | 7 |
| Journal | Circulation Research |
| Volume | 78 |
| Issue number | 2 |
| State | Published - Feb 1996 |
Fingerprint
Keywords
- absorption
- blood flow
- intestine
- nitric oxide
- oxygen use
- sodium
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
Intestinal absorption of sodium and nitric oxide-dependent vasodilation interact to dominate resting vascular resistance. / Bohlen, H.; Lash, Julia M.
In: Circulation Research, Vol. 78, No. 2, 02.1996, p. 231-237.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Intestinal absorption of sodium and nitric oxide-dependent vasodilation interact to dominate resting vascular resistance
AU - Bohlen, H.
AU - Lash, Julia M.
PY - 1996/2
Y1 - 1996/2
N2 - 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.
AB - 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.
KW - absorption
KW - blood flow
KW - intestine
KW - nitric oxide
KW - oxygen use
KW - sodium
UR - http://www.scopus.com/inward/record.url?scp=0030034946&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030034946&partnerID=8YFLogxK
M3 - Article
C2 - 8575066
AN - SCOPUS:0030034946
VL - 78
SP - 231
EP - 237
JO - Circulation Research
JF - Circulation Research
SN - 0009-7330
IS - 2
ER -