Key role of aldosterone and pericryptal myofibroblast growth in colonic permeability.

When sodium intake diminishes, both the kidney and distal colon contribute directly to sodium homeostasis. In response to a diet with low amounts of sodium, the body hormonal profile changes to produce different effects on crypt-colon permeability and absorption and in the pericryptal sheath surrounding distal colonic crypts. This adaptation produces an increase in Na absorption, a decreased crypt-wall permeability, and an activation of the growth of pericryptal myofibroblasts. The separate roles of the 2 main hormones implicated in the process, aldosterone and angiotensin II, until now have been unclear. Experiments conducted on adrenalectomized rats on low- and high-sodium diets, implanted with osmotic pumps perfusing either aldosterone or angiotensin II, allow us to discriminate between the effects of these hormones. In the distal colon, aldosterone acts as a trophic agent on the myofibroblasts layer and is the key hormone controlling colonic permeability, but angiotensin II alone has no discernable direct role in the process.