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Fluid transfer by isolated everted sacs of rat jejunum, ileum and intact colon prepared from adrenalectomized-nephrectomized rats 48 h after operation was reduced when compared with that of sacs prepared from untreated controls (P < 0\m=.\001).Angiotensin at 10\ m=-\ 10 g/ml significantly (P < 0\m=.\01) stimulated fluid transfer by intestinal sacs prepared from the adrenalectomized-nephrectomized rats; all three regions of gut were equally sensitive.Fluid transfer was similarly reduced in stripped colon sacs prepared from adrenalectomized-nephrectomized rats. Angiotensin had a dose-dependent biphasic action on fluid transfer by stripped colon sacs: low concentrations (10\m=-\11 and 10\m=-\12g/ml) stimulated (P < 0\m=.\05), whilst high concentrations (10\ m=-\ 9 and 10\m=-\8 g/ml) inhibited fluid transfer (P < 0\m=.\01).Histological examination of the colon preparations showed that the stripping procedure removed the ganglia, indicating that both angiotensin effects were due to direct action on the colon mucosa.The significance of these results is discussed in relation to the role of angiotensin in the control of salt and fluid transport by the mammalian kidney and other epithelial tissues.

SUMMARY1. A method has been described for the measurement of fluid transport by rat jejunum in vivo over two consecutive 30 min periods.2. Subpressor infusion rates of angiotensin (0.59 ng/kg per minute) stimulate fluid transport, while high (pressor) infusion rates (590 ng/kg per minute) inhibit fluid absorption.3. Both the inhibitory and stimulatory effects of angiotensin on fluid transport are not accompanied by any change in the transmural p.d., total blood flow to the jejunum or distribution of blood flow within the wall of the jejunum.4. These results are discussed in relation to the mechanism of action of angiotensin on fluid transport and its role in sodium and water homoeostasis.

The effect of phlorrhizin in inhibiting glucose absorption from the intestine both in vivo and in vitro is well established, but the mode of action is still un-known. The present work was undertaken in an attempt to locate the site of action of phlorrhizin in the intestine. It was done concurrently with the experiments using a different technique recently reported by Parsons, Smyth & Taylor (1958) and supports theif conclusion that one action of phlorrhizin is to prevent the entry of glucose into the epithelial cells from the mucosal side. A preliminary account has been given by Newey, Parsons & Smyth (1957). METHODSThe general principle of the experiments was to incubate segments of intestine aerobically in solutions containing 14C-uniformly-labelled glucose, to examine the radioactivity of the metabolic C02, and hence to determine whether glucose had penetrated into the cells. The intestinal preparation used was that of Wiseman (1953) as modified by Smyth & Whaler (1953). White rats weighing 200-300 g were anaesthetized with pentobarbitone sodium. The intestine was removed, and three segments of small intestine, each approximately 16 cm in length, taken from the jejunal end were fixed to the apparatus. The intestine was suspended in 25 ml. Ringer-phosphate solution (Krebs, 1933) containing 200 mg glucose/100 ml., and 40 ml. of the same solution was also circulated through the lumen of the intestinal segments. These solutions are referred to as the serosal and mucosal fluids respectively. Samples of the mucosal and serosal fluids were taken for analysis at the end of the experiments. In the radioactive experiments 14C-labelled glucose was added to either the mucosal or serosal fluid and in some cases to both. During the experiment the metabolic C02 was collected as BaCO3 as described by Smyth & Whaler (1953), the total amount of C02 was measured and also the radioactivity of the BaCO3. The activity of the glucose was determined by combustion and conversion to BaCO.. From the total amount of CO2 produced, the activity of the BaCO3 obtained from this, and the activity of the BaCO2 from the labelled glucose used, the amount of 14CO2 was calculated. Determinations were thus made of the metabolic C02derived from the glucose in the mucosal or serosal fluids. Further experiments were done in which phlorrhizin was added in various concentrations to the mucosal or serosal fluids, and the effect of this on the production of 14CO2 was measured. In order to allow time for the inhibitor to act the phlorrhizin was added 15 min before the labelled glucose, and therefore in the control experiments without phlorrhizin the preparation was incubated for 15 min before the labelled glucose was added.6-2