Sodium sensitive sites in the gastrointestinal tract stimulate natriuresis

Abstract

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. 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. 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. 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.