Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia.
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.
D000818:Animals; D001808:Blood Vessels / Q000503:physiopathology*; D006940:Hyperemia / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000503:physiopathology*; D007422:Intestines / Q000098:blood supply*; D008297:Male; D008839:Microelectrodes; D009994:Osmolar Concentration; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000502:physiology*; D013997:Time Factors
D012964:Sodium