The influence of bovine growth hormone and human placental lactogen on intestinal absorption was compared with that of ovine prolactin. Administration of each of these hormones in vivo daily for 2 days, resulted in increased fluid and electrolyte transport by the rat intestine, as measured in vitro. Hypophysectomy causes a fall in fluid and ion absorption in the rat jejunum but these changes are prevented by growth hormone treatment. Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Growth hormone also significantly increased fluid, sodium and chloride transport in the colon. Treatment of hypophysectomized rats with human placental lactogen enhanced fluid and ion transport in the jejunum; however, it failed to restore normal potassium transport in the ileum and colon at the 1 mg daily dose level. Growth hormone and human placental lactogen appear to affect jejunal water and electrolyte transport in the same manner as occurs with prolactin, possibly by influencing active ion transport.

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Mucosal fluid, sodium and chloride transfer were measured in everted sacs of rat, guinea-pig and hamster jejunum, and in rat ileum and colon, and in guinea-pig gall bladder. After treatment of the animal with ovine prolactin, a highly significant enhancement of fluid and NaCl absorption was observed in rat, hamster and guinea-pig jejunum. Prolactin treatment caused a significant increase in fluid and NaCl transfer in rat ileum, but not in gui nea\x=req-\ pig ileum or rat colon. Prolactin administration had no consistent effect on fluid and NaCl absorption by the guinea-pig gall bladder. The several regions of the mammalian gut appear to differ in their responsiveness to prolactin.

The influence of administration of ovine prolactin in vivo on intestinal fluid and ion transport in vitro was investigated using intact and hypophysectomized male rats. Prolactin administration significantly stimulated fluid, sodium,potassium, calcium, magnesium and chloride transport across everted jejunal sacs. The last two ions were affected less than the others. Hypophysectomy caused a significant decrease in fluid and sodium absorption, but prolactin treatment for 2 days restored normal absorption rates but not uniformly in all sacs. Prolactin action on fluid and sodium absorption showed a dose-dependent tendency, maximal stimulation resulting from administration of 1.0 to 2.0 mg prolactin daily; higher doses failed to elicit significant response. The stimulatory action of prolactin was inhibited by a simultaneous administration of vasopressin which when given alone had no effect on intestinal absorption. In the absence of glucose or in the presence of phlorizin, fluid transport was inhibited, the reduction being more dramatic in the presence of phlorizin. Similarly, either application of ouabain or partial replacement of sodium with isotonic choline chloride reduced fluid transport. Although these in vitro treatments nullified the stimulatory effects of prolactin, only phlorizin and ouabain significantly decreased sodium transport. These results suggest that the effects of prolactin on intestinal transport may be dependent on increased movement of sodium.

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