Electrical activity and sodium transfer across in vitro pig placenta.

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.