Decidual renin secretion is modulated by endothelial cells.

Because decidual renin may regulate uterine blood flow and decidual-endothelial cell proximity exists, we examined the modulation of decidual renin secretion by endothelial cells. Primary human decidual cell cultures were established. The effect of endothelial cells was studied by decidual-endothelial cocultures. Human umbilical endothelial cells were plated in half of the wells containing decidual cells and were then incubated for 24 h in serum-free media. The effect of endothelial cells was also studied by examining cAMP-mediated renin secretion using 10(-5) M forskolin under standardized conditions. We also examined the role of cell-to-cell contact by coculturing endothelial cells directly on decidual cultures and on cell inserts placed in decidual culture wells. The media were assayed for renin by radioimmunoassay (RIA) for angiotensin I (AI) after AI generation under standardized conditions. Statistical differences were analyzed by two-way analysis of variance (ANOVA) with randomized complete block design. Basal renin secretion, expressed as mean +/- SEM was 10.3 +/- 1.0 ng AI/ml/h. cAMP stimulation increased this to 15.5 +/- 1.3 ng AI/ml/h, P < 0.02. Coculture with vascular endothelium increased renin secretion to 24.3 +/- 2.4 ng AI/ml/h, P < 0.001. cAMP stimulation in cocultures increased renin secretion to 38.0 +/- 4.4 ng AI/ml/h, P < 0.002. There was no effect on cell growth as examined by total protein concentrations by coculturing or by cAMP. There was no increase in renin secretion when endothelial cells were cocultured using cell well inserts. Our data suggest that decidual renin secretion is increased by the presence of endothelial cells in direct contact with decidual cells. This supports a concept that in vivo-decidual-endothelial interaction may modulate decidual renin secretion and thereby influence regulation of uterine blood flow.