AJP - Regulatory, Integrative and Comparative Physiology, Vol 250, Issue 3 474-R484, Copyright © 1986 by American Physiological Society
Electrical activity and sodium transfer across in vitro pig placenta
C. P. Sibley, B. S. Ward, J. D. Glazier, W. M. Moore and R. D. Boyd
Electrical activity generated by pieces of pig placenta, taken from
anesthetized animals and mounted in Ussing chambers, has been investigated.
Ten minutes after the start of voltage clamping, potential difference (PD;
fetal side positive, open circuit), short circuit current (SCC), and
resistance were 5.9 +/- 0.4 (SE) mV, 8.6 +/- 0.5 microA X cm-2, and 720 +/-
45 omega X cm2, respectively (n = 50). Ouabain (10(-4) M) added to the
fetal side caused a maximum decline in PD and SCC from the time of addition
of -3.7 +/- 0.98 mV and -3.9 +/- 1.4 microA X cm-2 (n = 6); epinephrine
(10(-5) M) added to the fetal side caused increases of +1.0 +/- 0.2 mV and
+4.0 +/- 1.4 microA X cm-2, respectively (n = 14). Drug concentrations for
50% maximum response for the effect of a series of adrenergic agonists on
SCC were (in M) isoproterenol 1.2 +/- 0.05 X 10(-8), norepinephrine 6.1 +/-
0.3 X 10(-8), epinephrine 2.4 +/- 0.1 X 10(-7), and phenylephrine 4.7 +/-
0.2 X 10(-5), suggesting the involvement of fetally oriented
beta-adrenergic receptors. Fetal epinephrine (10(-5) M) also stimulated net
Na+ flux (Jnet) toward the fetal side to an extent equal to its effect on
SCC. In control experiments Jnet was small but was inhibited by fetal side
ouabain (10(-4) M) to produce a maternally directed Jnet, significantly
different to the SCC. Replacement of Na+ by choline reduced SCC markedly
but did not abolish it. In the absence of Na+, epinephrine had no effect on
SCC. These results suggest that active Na+ transfer is not completely
responsible for the control electrical activity of pig placenta.
Epinephrine, however, modulates SCC entirely by stimulating net Na+
transfer toward the fetal side.
