Shillingford J M, Calvert D T, Beechey R B, Shennan D B
Hannah Research Institute, University of Wales, Aberystwyth, UK.
Exp Physiol. 1996 Mar;81(2):273-84. doi: 10.1113/expphysiol.1996.sp003931.
Inorganic orthophosphate (Pi) transport, using 32P-labelled orthophosphate as tracer, by lactating rat mammary tissue has been examined using both tissue explants and the intact perfused gland. Pi uptake was predominantly via a Na+ -dependent pathway. Li+, however, unlike choline, was able to partially substitute for Na+. In addition, Pi release from tissue explants preloaded with 32Pi was stimulated by reversing the Na+ gradient. Thus transferring mammary explants from a buffer containing Na+ to one which was Na+ free (choline replacement) doubled the Pi efflux rate constant. The uptake of Pi by tissue explants was saturable with respect to external Pi, having apparent K(m) and V(max) values of 1.13 mM and 3.36 mmol (kg cell water)-1 (15 min)-1, respectively. The stimulation of Pi uptake by tissue explants by external Na+ was also saturable; the K(m) for Na+ was 9.7 mM. These results, taken together, suggest that the Na+ -dependent pathway is a Na+ -Pi cotransport mechanism. The transport of Pi by the perfused lactating rat mammary gland was examined using a rapid, paired-tracer dilution technique. Pi uptake by the perfused gland was found to be Na+ dependent and displayed saturable kinetics. The results suggest that the Na+ -Pi cotransporter is situated at the basolateral aspect of the secretory cells. The release of Pi from preloaded tissue explants was trans-accelerated by external Pi but not by Cl- or SO4(2-). However, external Pi stimulated Pi efflux with low affinity.
