The acute effect of intraperitoneally administered
prolactin (0.2, 0.4, and 0.6 mg/kg
body weight) on passive
calcium transport in duodenum, proximal jejunum, and ileum of sexually mature female Wistar rats was investigated by using an in vivo perfusion technique. Test
solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20;
D-glucose, 11;
sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 microCi 45CaCl2 (1 Ci = 37 GBq) was perfused through the 10-cm intestinal loop for 60 min. Results showed that 0.4 mg
prolactin/kg
body weight significantly increased duodenal net Ca absorption (net Ca) from 23.81 +/- 1.84 to 30.56 +/- 1.57 mmol/g dry weight (p < 0.05) by stimulating the lumen to plasma
calcium flux (CaL-P). The jejunum responded to 0.2, 0.4, and 0.6 mg
prolactin/kg
body weight by reversing from net Ca absorption of 18.60 +/- 1.70 mmol/g dry weight to net secretion of -3.30 +/- 1.56, -10.39 +/- 2.21, and -11.79 +/- 2.04 mmol/g dry weight (p < 0.01), respectively, as a result of a dose-dependent increase in plasma to lumen
calcium flux (CaP-L).
Calcium fluxes in the ileum on the other hand did not respond to
prolactin. There was a close correlation between net water flux and net
calcium flux in all three intestinal segments under basal condition regardless of the
luminal sodium concentration. However, this correlation was lost after
prolactin administration, which while having no effect on net water flux, altered the duodenal and jejunal
calcium fluxes. By varying the
luminal concentration of
sodium, it was found that the stimulatory effect of 0.4 mg
prolactin/kg
body weight on the duodenal CaL-P was reduced when compared with control, i.e., 17.84 +/- 0.91 vs. 26.64 +/- 1.05 mmol/g dry weight at a
sodium concentration of 180 mM, and 14.48 +/- 0.99 vs. 20.12 +/- 1.34 mmol/g dry weight at a
sodium concentration of 140 mM. At a
sodium concentration of 80 mM, the
prolactin effect was absent. Since duodenal Na(+)-K+
ATPase activity was increased by
prolactin from 3.77 +/- 0.16 to 4.95 +/- 0.30 mumol Pi.mg-1 protein.h-1 (p < 0.05),
sodium dependency of the
prolactin-enhanced lumen to plasma
calcium flux may be related to both
sodium-induced water flow and
calcium-
sodium exchange across the basolateral membrane. Thus, it was postulated that under basal condition, net
calcium transport in the small intestine occurred with the
sodium-induced water transport along the paracellular pathway. However, after
prolactin administration, this association was lost.
Prolactin-enhanced lumen to plasma
calcium flux in the duodenum was
sodium dependent and involved the Na(+)-K+
ATPase activity. In the proximal jejunum,
prolactin stimulated plasma to lumen
calcium flux, but the mechanism was not known.