Epidemiological studies indicate that a reduced birth weight and enlarged placenta increase the likelihood of human cardiovascular disease later in life. The relative importance of fetal versus maternal factors in these phenomena is not known. To assess the relative role of genotypic versus environmental factors in this effect, we examined whether the altered fetal and placental growth rates and amniotic fluid volume of spontaneously hypertensive rat (SHR) fetuses of the Okamoto strain, are modified by gestation in normotensive Wistar–Kyoto (WKY) rat mothers and vice versa.
One-day-old SHR embryos were gestated for 16 days in either SHR or WKY recipients. Similarly, 1-day-old WKY rat embryos were gestated for 16 days in either SHR or WKY surrogates. At 16 days, fetal and placental weights were recorded. Paternal and maternal donor and recipient blood pressures, maternal body weight and average litter size within the four groups were also studied.
One cell SHR and WKY embryos were harvested from timed matings and transferred to psuedopregnant mothers of the same or opposite strain. Timed matings required routine vaginal smears for the detection of proestrus and the presence of sperm following overnight matings. Harvested embryos were temporarily maintained in culture medium in a 37°C incubator until injection into the oviduct of recipients. Blood pressures were meaured using indirect, tail-cuff plethysmography and a computerized data acquisition system.
SHR fetal and placental weights at 16 days gestation were significantly lower than WKY fetal and placental weights, irrespective of maternal strain. At 16 days of gestation, the fetal and placental weights of SHR fetuses gestated in WKY rat surrogate mothers (0.21 ± 0.01 g and 0.19 ± 0.01 g, respectively) were not significantly different from those of SHR gestated in a surrogate SHR mother (0.21 ± 0.01 g and 0.18 ± 0.01 g, respectively). Similarly, the fetal and placental weights of WKY fetuses gestated in a WKY rat (0.27 ± 0.01 g and 0.25 ± 0.01 g, respectively) were unaltered by gestation in a SHR recipient (0.25 ± 0.01 g and 0.23 ± 0.01 g, respectively). The amniotic fluid volumes of SHR gestated in WKY rats and those of WKY fetuses gestated in SHR were not significantly different to each other (0.37 ± 0.01 ml versus 0.38 ± 0.01 ml, respectively) and were intermediate between the values for SHR and WKY fetuses gestated in a mother of the same strain (0.34 ± 0.01 ml versus 0.44 ± 0.02 ml, respectively).
The SHR fetus exhibited reduced growth rate and placental size irrespective of maternal surrogate strain, suggesting that these measures are likely to be determined by the fetus or the placenta and, presumably, are independent of maternal blood pressure or altered electrolyte and hormonal milieu.