Increased intestinal absorption in the rat caused by sodium lauryl sulphate, and its possible relation to the cAMP system

Abstract

The increases in the absorption of ouabain, phenolsulphonphthalein and pralidoxime caused by 17 mM sodium lauryl sulphate (SLS) from jejunal loops of anaesthetized rats were significantly reduced if sodium and chloride (Briseid et al., 1974) or chloride and bicarbonate were replaced by other ions in the loop fluid. Separate substitutions of sodium, chloride of bicarbonate did not significantly alter the SLS-caused absorption, except that the substitution of choline for sodium reduced the absorption of pralidoxime, both in the presence and in the absence of SLS. The increases in the absorption of phenolsulphonphthalein and pralidoxime caused by SLS were potentiated by theophylline (25 mM) and reduced by imidazole (25 mM). The addition of dibutyryl cyclic AMP (2.5 mM) to the loop fluid increased this absorption of the test substances. This effect was reduced by imidazole, but under the experimental conditions it was not potentiated by theophylline. Determinations of cyclic AMP in the rat intestinal mucosa showed that the level of this substance was significantly higher in the presence than in the absence of SLS. The experimental conditions were as described for the absorption experiments. It is concluded that the data obtained support the idea of an increased level of cyclic AMP as the main basis for the effect of SLS on the absorption.

Net Sodium and Glucose Transport in the Jejunum, Ileum and Colon of Anaesthetized Rats in Response to Intraluminal Theophylline and Anionic Surfactants

“…In the present work, these two possibilities have been explored by studying the influence of theophylline and DOSS on the abovementioned absorption processes in vivo. Another anionic surfactant, dodecylsulphate (=DDS), was also included, since this drug may induce some increased formation of CAMP (Briseid et al 1976(Briseid et al & 1977Sund & Hillestad 1981). A short account of this study has been presented elsewhere (Sund & Olsen 1978).…”

Human colonic adenylate cyclase: effects of bile acids

“…It is therefore intriguing to speculate that the increase of adenylate cyclase activity and of colonic mucosal cAMP following incubation with bile acids may be regarded as a non-specific effect of this compound. In this context it is interesting to note that the intracellular concentrations of CAMP in the intestinal mucosa could be nonspecifically increased in the presence of other surfactants, too [12,131 . Our results therefore suggest that bile acid induced diarrhoea is not associated with activation of the membrane-bound adenylate cyclase, at least in man.…”

Intestinal filtration as a consequence of increased mucosal hydraulic permeability

“…The results obtained from short circuit experiments basically underline that DC and OP do not stimulate intestinal ionic secretion. This has been suggested for cholera toxine (Kimberg et al, 1971), vasoactive intestinal polypeptide (Schwartz et al, 1974;Carter et al, 1978, Gaginella et al, 1978, escherichia coli toxine (Banwell and Sherr, 1973), certain prostaglandines (Kimberg et al, 1971 ;Gaginella et al, 1978), fatty acids (Bright-Asare and Binder, 1973), deoxycholate (Binder etal., 1975;Conley et al, 1976), laxative acting surfactants such as sodium lauryt sulfate (Briseid et al, 1976), sodium sulfosuccinate (Donowitz and Binder,t975). Chloride secretion is not caused by short-circuiting the intestine per se since Binder and Rawlins (1973 a) found chloride absorption in the Ussing-chamber under these conditions.…”