Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia.

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Abstract

The coupled active transport of Na+ with sugars and amino acids could cause intestinal villus interstitial hyperosmolarity, which contributes to absorptive hyperemia. However, for the villus hyperosmolarity to cause a major vascular response, a mild-to-moderate hyperosmolarity must occur in the vicinity of the major resistance vessels of the submucosa. Interstitial Na+ activity was measured throughout the small intestinal wall of rats with monensin ion-selective electrodes during glucose absorption. In the upper half of villi, the resting [Na+] was 201 +/- 5 (SE) mM and increased to 267 +/- 6 mM during luminal exposure to 25-300 mg/100 ml glucose. The submucosal resting [Na+] was 144 +/- 1 mM and increased to 177 +/- 3 mM during luminal glucose exposure. The time courses of Na+ appearance and submucosal arterial dilation were almost identical. Calculations of tissue osmolarity indicate an increase in villus osmolarity of 150-200 mosM and 79-90 mosM in the submucosa during glucose absorption. The data are interpreted to indicate that villus hyperosmolarity during glucose absorption increased submucosal osmolarity and a naturally occurring osmotic dilatory component of absorptive hyperemia could exist.

Original languageEnglish
JournalThe American journal of physiology
Volume242
Issue number5
StatePublished - May 1982
Externally publishedYes

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Hyperemia
Blood Vessels
Glucose
Osmolar Concentration
Ion-Selective Electrodes
Sugar Acids
Monensin
Active Biological Transport
Dilatation
Amino Acids

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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abstract = "The coupled active transport of Na+ with sugars and amino acids could cause intestinal villus interstitial hyperosmolarity, which contributes to absorptive hyperemia. However, for the villus hyperosmolarity to cause a major vascular response, a mild-to-moderate hyperosmolarity must occur in the vicinity of the major resistance vessels of the submucosa. Interstitial Na+ activity was measured throughout the small intestinal wall of rats with monensin ion-selective electrodes during glucose absorption. In the upper half of villi, the resting [Na+] was 201 +/- 5 (SE) mM and increased to 267 +/- 6 mM during luminal exposure to 25-300 mg/100 ml glucose. The submucosal resting [Na+] was 144 +/- 1 mM and increased to 177 +/- 3 mM during luminal glucose exposure. The time courses of Na+ appearance and submucosal arterial dilation were almost identical. Calculations of tissue osmolarity indicate an increase in villus osmolarity of 150-200 mosM and 79-90 mosM in the submucosa during glucose absorption. The data are interpreted to indicate that villus hyperosmolarity during glucose absorption increased submucosal osmolarity and a naturally occurring osmotic dilatory component of absorptive hyperemia could exist.",
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T1 - Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia.

AU - Bohlen, H.

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N2 - The coupled active transport of Na+ with sugars and amino acids could cause intestinal villus interstitial hyperosmolarity, which contributes to absorptive hyperemia. However, for the villus hyperosmolarity to cause a major vascular response, a mild-to-moderate hyperosmolarity must occur in the vicinity of the major resistance vessels of the submucosa. Interstitial Na+ activity was measured throughout the small intestinal wall of rats with monensin ion-selective electrodes during glucose absorption. In the upper half of villi, the resting [Na+] was 201 +/- 5 (SE) mM and increased to 267 +/- 6 mM during luminal exposure to 25-300 mg/100 ml glucose. The submucosal resting [Na+] was 144 +/- 1 mM and increased to 177 +/- 3 mM during luminal glucose exposure. The time courses of Na+ appearance and submucosal arterial dilation were almost identical. Calculations of tissue osmolarity indicate an increase in villus osmolarity of 150-200 mosM and 79-90 mosM in the submucosa during glucose absorption. The data are interpreted to indicate that villus hyperosmolarity during glucose absorption increased submucosal osmolarity and a naturally occurring osmotic dilatory component of absorptive hyperemia could exist.

AB - The coupled active transport of Na+ with sugars and amino acids could cause intestinal villus interstitial hyperosmolarity, which contributes to absorptive hyperemia. However, for the villus hyperosmolarity to cause a major vascular response, a mild-to-moderate hyperosmolarity must occur in the vicinity of the major resistance vessels of the submucosa. Interstitial Na+ activity was measured throughout the small intestinal wall of rats with monensin ion-selective electrodes during glucose absorption. In the upper half of villi, the resting [Na+] was 201 +/- 5 (SE) mM and increased to 267 +/- 6 mM during luminal exposure to 25-300 mg/100 ml glucose. The submucosal resting [Na+] was 144 +/- 1 mM and increased to 177 +/- 3 mM during luminal glucose exposure. The time courses of Na+ appearance and submucosal arterial dilation were almost identical. Calculations of tissue osmolarity indicate an increase in villus osmolarity of 150-200 mosM and 79-90 mosM in the submucosa during glucose absorption. The data are interpreted to indicate that villus hyperosmolarity during glucose absorption increased submucosal osmolarity and a naturally occurring osmotic dilatory component of absorptive hyperemia could exist.

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