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

Research output: Contribution to journalArticle

18 Citations (Scopus)

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 dilatation 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
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume11
Issue number5
StatePublished - 1982

Fingerprint

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

ASJC Scopus subject areas

  • Physiology

Cite this

@article{1ded6baa98264d0d94126c08682fe327,
title = "Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia",
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 dilatation 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.",
author = "H. Bohlen",
year = "1982",
language = "English",
volume = "11",
journal = "American Journal of Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia

AU - Bohlen, H.

PY - 1982

Y1 - 1982

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 dilatation 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 dilatation 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.

UR - http://www.scopus.com/inward/record.url?scp=0019955254&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019955254&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0019955254

VL - 11

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0193-1857

IS - 5

ER -