C. P. Sibley

Amino acid (system A) transporter activity in microvillous membrane vesicles from the placentas of appropriate and small for gestational age babies

ABSTRACT: Although a number of causes of poor fetal growth are known, the involvement of placental transport proteins in the etiology of growth retardation is not understood. The aim of this study was to investigate the activity of the system A amino acid transporter and the Na+/H+ exchanger in vesicles isolated from the microvillous membrane of the syncytiotrophoblast of placentas of appropriate and small for gestational age babies. There were no biochemical differences between the membranes from the two groups of placentas, and there was no difference in the activity of the Na+/H+ exchanger. The initial rate of uptake of methylaminoisobutyric acid (a nonmetabolizable amino acid analogue) was 63% lower in vesicles from placentas of small for gestational age babies. Kinetic analysis of the system A transporter (utilized by methylaminoisobutyric acid) showed that the Vmax in the vesicles from placentas of small for gestational age babies (0.24 ± 0.03 nmol/mg protein/30 s, n = 5) was significantly lower than that in vesicles from placentas of appropriate for gestational age babies (0.64 ± 0.09 nmol/mg protein/30 s, n = 4, p < 0.001), whereas the Km was not different between the two groups. It is concluded that there is an abnormality of system A amino acid transporter function in placentas of small for gestational age babies.

Calbindin-D9K gene expression in rat chorioallantoic placenta is not regulated by 1,25-dihydroxyvitamin D3.

ABSTRACT: The aim of this study was to investigate whether 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the active metabolite of vitamin D, regulates the expression of rat placental calbindin-D9K mRNA. One group of rats (-D) was fed a vitamin D-deficient diet before and during pregnancy, whereas a second group (+D) was fed a vitamin D-replete diet over the same period. Animals were killed on d 21 of gestation, and plasma concentrations of 1,25(OH)2D3 for +D and –D animals were significantly (p < 0.05) different (260 ± 78 and 39 ± 8 pM in maternal plasma and 122 ± 39 and 42 ± 10 pM in fetal plasma, respectively; mean ± SE, n = 4–5). Vitamin D deficiency had no effect on placental weight, fetal weight, fetal ashed weight, fetal calcium accretion, or the maternofetal calcium gradient. Hybridization of RNA from maternal duodena (used as a positive control tissue) and placentas of +D and –D rats with a rat calbindin-D9K cDNA revealed a single 0.6-kb transcript in both tissues. The abundance of this transcript was markedly lower (p = 0.06) in the duodena of –D compared with +D rats (mean change –68 ± 9%) but there was no difference between the placentas of the two groups (mean change + 13 ± 22%). These changes were significantly (p < 0.05) different between the two tissues and the response of each tissue to vitamin D deficiency was significantly different (p < 0.01). These data indicate that 1,25(OH)2D3 does not regulate the expression of calbindin-D9K mRNA in rat placenta.

Site of catecholamine modulation of feto-maternal electric potential difference in the pig

Feto‐maternal vascular (PD(F‐M)) and amniotic maternal (PD(A‐M)) potential differences were measured simultaneously on seven occasions in six conscious pigs of 100–106 days gestation. Resting values of PD(F‐M) and PD(A‐M) were not significantly different although the range was wide. Fetal intravascular injection of 20 microg adrenaline, but not of saline, was associated with a prompt reversible change, of equal magnitude, in both PD(F‐M) and PD(A‐M). In some experiments polarity was reversed. Feto‐amniotic potential difference did not change. There was no change in fetal plasma K+ and Na+ concentrations. Because of the simultaneous and equal alterations in PD(F‐M) and PD(A‐M) following adrenaline and the anatomical configuration of the pig conceptus, we conclude that the catecholamine modifiable component of PD(F‐M) is generated by electrogenesis in the pig placenta, probably by its chorionic (trophoblastic) cell layer.