Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis

<p>In 1975 Lennane and colleagues studied the effects of oral sodium loading on renal function by gavage in rabbits and oral ingestion in humans. (Lennane et al, 1975a; Lennane et al, 1975b) The renal response to orally administered sodium was notably more significant than the natriuresis foll...

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Main Author: Williamson, Kara Nadine
Other Authors: Evered, Mark
Format: Others
Language:en
Published: University of Saskatchewan 2012
Online Access:http://library.usask.ca/theses/available/etd-08132012-131441/
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spelling ndltd-USASK-oai-usask.ca-etd-08132012-1314412013-01-08T16:35:34Z Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis Williamson, Kara Nadine <p>In 1975 Lennane and colleagues studied the effects of oral sodium loading on renal function by gavage in rabbits and oral ingestion in humans. (Lennane et al, 1975a; Lennane et al, 1975b) The renal response to orally administered sodium was notably more significant than the natriuresis following intravenous infusion of the same sodium load, suggesting to the authors that the response was initiated by a gastric sodium sensor. There is no evidence to support the sodium sensor described by Lennane and colleagues is located in the stomach, however a sensor may be located somewhere along the gastrointestinal tract. The gastrointestinal tract is an ideal location for a sodium sensor to alert the body to impending changes in plasma sodium concentration. A gastrointestinal sodium sensor capable of monitoring ingested sodium loads and controlling urinary sodium excretion would be a favourable contributor to body fluid balance and body sodium homeostasis.</p> <p>Male Long-Evans rats with permanent bladder and gastrointestinal cannulas were used to determine an approximate location for the gastrointestinal site causing the greatest increase in urinary sodium excretion following infusion of various solutions. Animals remained unrestrained for the 200 minute period of the experiment while urine samples were collected every 20 minutes. Following a 60 minute baseline period, one milliliter of 0.15M (isotonic) sodium chloride, 0.5M (hypertonic) sodium chloride or a 0.5M (hypertonic) mannitol solution was infused into the stomach, duodenum, jejunum, ileum, or colon over a twenty minute infusion period through a silicon cannula. Urine samples were analyzed for sodium content to determine if a sensor in the intestines initiated a natriuretic reflex.</p> <p>Results from these experiments indicate the small intestine promotes the largest stimulation of natriuresis following infusion of 0.5M NaCl into the duodenum, the ileum and the jejunum. Hypertonic sodium chloride infusion activated the intestino-renal response whereas isotonic saline or equimolar mannitol did not, suggesting sensitivity of the gut to sodium concentration but not osmolar concentration.</p> <p>The natriuresis occurred promptly following infusion suggesting a neural component to the intestino-renal response. A humoral component may also be involved in the intestino-renal reflex since sodium excretion remained significantly greater than baseline for an hour following the infusion period.</p> Evered, Mark Wollin, Armin University of Saskatchewan 2012-08-13 text application/pdf http://library.usask.ca/theses/available/etd-08132012-131441/ http://library.usask.ca/theses/available/etd-08132012-131441/ en unrestricted I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report.
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description <p>In 1975 Lennane and colleagues studied the effects of oral sodium loading on renal function by gavage in rabbits and oral ingestion in humans. (Lennane et al, 1975a; Lennane et al, 1975b) The renal response to orally administered sodium was notably more significant than the natriuresis following intravenous infusion of the same sodium load, suggesting to the authors that the response was initiated by a gastric sodium sensor. There is no evidence to support the sodium sensor described by Lennane and colleagues is located in the stomach, however a sensor may be located somewhere along the gastrointestinal tract. The gastrointestinal tract is an ideal location for a sodium sensor to alert the body to impending changes in plasma sodium concentration. A gastrointestinal sodium sensor capable of monitoring ingested sodium loads and controlling urinary sodium excretion would be a favourable contributor to body fluid balance and body sodium homeostasis.</p> <p>Male Long-Evans rats with permanent bladder and gastrointestinal cannulas were used to determine an approximate location for the gastrointestinal site causing the greatest increase in urinary sodium excretion following infusion of various solutions. Animals remained unrestrained for the 200 minute period of the experiment while urine samples were collected every 20 minutes. Following a 60 minute baseline period, one milliliter of 0.15M (isotonic) sodium chloride, 0.5M (hypertonic) sodium chloride or a 0.5M (hypertonic) mannitol solution was infused into the stomach, duodenum, jejunum, ileum, or colon over a twenty minute infusion period through a silicon cannula. Urine samples were analyzed for sodium content to determine if a sensor in the intestines initiated a natriuretic reflex.</p> <p>Results from these experiments indicate the small intestine promotes the largest stimulation of natriuresis following infusion of 0.5M NaCl into the duodenum, the ileum and the jejunum. Hypertonic sodium chloride infusion activated the intestino-renal response whereas isotonic saline or equimolar mannitol did not, suggesting sensitivity of the gut to sodium concentration but not osmolar concentration.</p> <p>The natriuresis occurred promptly following infusion suggesting a neural component to the intestino-renal response. A humoral component may also be involved in the intestino-renal reflex since sodium excretion remained significantly greater than baseline for an hour following the infusion period.</p>
author2 Evered, Mark
author_facet Evered, Mark
Williamson, Kara Nadine
author Williamson, Kara Nadine
spellingShingle Williamson, Kara Nadine
Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
author_sort Williamson, Kara Nadine
title Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
title_short Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
title_full Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
title_fullStr Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
title_full_unstemmed Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
title_sort sodium sensitive sites in the gastrointestinal tract stimulate natriuresis
publisher University of Saskatchewan
publishDate 2012
url http://library.usask.ca/theses/available/etd-08132012-131441/
work_keys_str_mv AT williamsonkaranadine sodiumsensitivesitesinthegastrointestinaltractstimulatenatriuresis
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