| Summary: | <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>
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