Net ion fluxes and zero flux limiting concentrations in rat upper colon and rectum during anaesthesia-induced aldosterone liberation

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Abstract
Thiobutabarbital anaesthetized and abdominally operated control rats develop high endogenous plasma levels of both aldosterone and corticosterone during the course of a 12 h experiment. This effect was used as a model for examining ‘acute’ steroid action (i) on net ion and water fluxes and (ii) on zero flux luminal limiting concentrations in rat upper colon (proximal 50% of large intestine) and rectum (distal 40%). Experiments of both kinds consisted of 8 independent 90 min measuring periods. In rectum net fluxes of Na, K, osmolytes (sum of all solutes) and water started at low levels around zero, began to rise about 2 h after plasma levels of aldosterone had increased, and reached plateau values around the 6th hour of anaesthesia. In upper colon, fluxes of Na, K, Cl, and osmolytes were high from the beginning and did not vary significantly with time. At zero flux conditions limiting concentrations of Na in the hormonally unstimulated phase of the experiment were 20±3 mM in upper colon and 22±3 mM in rectum. After maximal endogenous aldosterone liberation zero flux concentrations were 5.2 mM in upper colon and 2.2 mM in rectum, corresponding to luminal fluid to plasma ratios (LF/P) of 0.040 and 0.016, respectively. Amiloride reduced the maximal Na gradient in rectum to aLF/P of 0.3 but was not effective in upper colon and did not prevent the stimulating effect of aldosterone in this segment. Under all experimental conditions zero flow concentrations of K were higher than consistent with a solely passive distribution, indicating simultaneous passive and active secretion in both segments. In contrast to the findings of others, the luminal fluid remained isoosmolar with plasma in all zero flux experiments. Conclusions: Under acute elevation of steroid levels not higher than reached in a living animal the rectum varies net fluxes of Na, K, osmolytes, and water between zero and high rates. At this range of steroid levels, the upper colon practically does not respond with variations in net fluxes. Under zero flux conditions aldosterone acutely increases maximal Na gradients in rectum and, to a lesser degree, also in upper colon. Thus, acutely elevated aldosterone levels affect Na transport in upper colon and rectum by different mechanisms and intensities: in rectum, which is the most sensitive site of transport regulation, via an amiloridesensitive Na-pathway, and in upper colon, via an amiloride-insensitive pathway.

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