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Abdominal arteries may have a greater relaxation response to bradykinin than uterine arteries in both pregnant and nonpregnant women. Researchers obtained omental (abdominal) and uterine muscle arteries from 22 pregnant and 27 nonpregnant women. Arteries were constricted with vasopressin, and then relaxed with bradykinin. Omental arteries relaxed more than did uterine muscle arteries in both pregnant and nonpregnant women. No difference was seen in the blood vessel relaxation response between pregnant and nonpregnant women.

A role for angiogenic growth factors in trophoblast invasion has been postulated. Directional motility (chemotaxis) is an important function of trophoblast cells. We have previously shown that vascular endothelial growth factor (VEGF) increases the random movement of trophoblast cells although placental growth factor (PlGF) has no effect. Heparin inhibited this effect of VEGF. Motility of trophoblast cells has been proposed to be mediated by a nitric oxide (NO) pathway. We hypothesized that VEGF but not PlGF would be chemotactic for trophoblast cells. Chemotaxis of a first trimester extravillous trophoblast cell line, SGHPL-4, and primary isolates of first trimester and term trophoblast cells was measured using a Boyden chamber. Initial experiments to optimize the time of the experiment and identify a positive control were performed. Subsequent experiments ran for 20h, used 0.5 per cent FBS or 10ng/ml PDGF as negative and positive controls and were performed in triplicate. VEGF (1, 10 and 100ng/ml±1μg/ml heparin or ±100μmL-NAME) and PlGF (1, 10, 100ng/ml) were tested. The chamber was placed in a 5 per cent CO2in air, 37°C incubator. The number of cells in the lower chamber were counted. There was a dose dependent increase in chemotactic motility of the SGHPL-4 cell line and term trophoblast cells in response to VEGF. PlGF had no effect on the movement of the first trimester trophoblast cell line but did increase the motility of the term trophoblast cells in a dose dependent manner. Heparin increased the cellular motility of both cell types alone. It also further enhanced the chemoactivity of VEGF on the term trophoblast cells but not the cell line. L-NAME did not affect the VEGF-stimulated motility of the first trimester cell line. However, in the term trophoblast cells L-NAME increased the directional cellular motility in the absence of, or in the presence of low concentrations of VEGF. In conclusion, the first trimester and term trophoblast cells appeared to respond differently to the various factors tested in the present study that may reflect differential cellular function as gestation progresses.

An angiotensin I-like substance has been detected in media after incubation of human chorion-decidua in vitro. The substance was identified as angiotensin I by gel filtration, ion exchange chromatography, and a specific antiserum to angiotensin I. The presence of angiotensin I in these incubates indicates that renin substrate may be either stored or synthesized by the tissue. The levels of angiotensin I produced during incubation were greater than could be explained by the action of renin on plasma substrate since the major part of the chorion-decidua is avascular. Previously chorion-decidua has been shown to contain large amounts of renin and to be capable of synthesizing both active and inactive forms of the enzyme in vitro; however, renin substrate has not been described in this tissue.

Tissues from the fetoplacental unit were incubated in medium E 199 at 0° C and following removal of the tissue were incubated at 37° C. Compared to control tissues held at 0° C, large quantities of angiotensin I, measured by means of specific radioimmunoassay, were detected in the media from both amnion and chorion-decidua while only small amounts were found in the media from placenta and umbilical cord. Following prior incubation with antirenin, the generation of angiotensin I was abolished in all tissues. These results indicate that both renin and its substrate are released into the media during incubation at 0° C and suggest the existence of a locally functioning renin-angiotensin system in certain tissues of the human female genital tract.