Hh. Wenzl et al., EFFECT OF FLUDROCORTISONE AND SPIRONOLACTONE ON SODIUM AND POTASSIUM LOSSES IN SECRETORY DIARRHEA, Digestive diseases and sciences, 42(1), 1997, pp. 119-128
The response of the colon to aldosterone is believed to be an importan
t adaptive mechanism to excessive sodium losses in diarrhea. However,
the degree to which mineralocorticoid activity actually influences fec
al output of sodium in people with diarrhea is unknown. To gain insigh
t into this question, 10 normal people were treated with placebo, flud
rocortisone (an aldosterone agonist), and spironolactone (an aldostero
ne antagonist) during three experimental periods lasting nine days. On
days 5-8, diarrhea was induced by ingestion of phenolphthalein. Diet
was controlled. Fecal sodium was 40 meq/day on placebo and 29 meq/day
on fludrocortisone, consistent with mineralocorticoid stimulation of i
ntestinal sodium absorption. However, contrary to our expectations, sp
ironolactone therapy was also associated with a fall in fecal sodium o
utput, to 28 meq/day. To explain this paradoxical effect of spironolac
tone, we suggest that sodium depletion caused by spironolactone's natr
iuretic action on the kidney caused the release of an unknown stimulan
t of intestinal sodium absorption, whose action more than overcame the
reduced colonic absorption resulting from inhibition of aldosterone a
ctivity by spironolactone. This interpretation implies that the intest
inal adaptation to sodium depletion in diarrhea involves both aldoster
one and an aldosterone independent factor, working in concert to reduc
e fecal sodium output.