Full expression of the exaggerated salt appetite of the spontaneously hypertensive rat requires a prenatal factor.

1. The spontaneously hypertensive rat (SHR) exhibits a lower bodyweight in utero and an exaggerated salt appetite post partum. To determine whether salt appetite is affected by the perinatal environment, we measured the salt appetite of embryo-cross-transferred SHR and Wistar Kyoto (WKY) rats at maturity. 2. One-cell embryos were collected from the oviducts of donor rats and transferred into the oviducts of recipients through the infundibulum. The salt appetite of the resultant female offspring for 0.10 and 0.15 mol/L saline was measured at 20-30 weeks of age. 3. Salt intake of SHR gestated in WKY rats was significantly lower than that of SHR gestated in SHR, while that of WKY rats gestated in SHR was higher than that of WKY rats gestated in WKY rats. 4. Therefore, some maternal factor plays a role in the development of the exaggerated salt appetite of the SHR. This factor is also able to affect the later salt appetite of WKY rat offspring born to SHR surrogates.

Amniotic fluid composition and fetal and placental growth rates in genetically hypertensive and normotensive rats.

Reduced birth weight has been observed in offspring of the spontaneously hypertensive rat (SHR) and in human hypertension. To determine which uterine factors might contribute to this fetal underdevelopment, fetal and placental growth rates and the volume and composition of amniotic fluid were measured in SHR and normotensive control Wistar Kyoto (WKY) rats during the final trimester of intra-uterine development. SHR and WKY fetuses were collected on Days 15-22 of pregnancy, and fetal and placental weight and amniotic fluid volume were recorded. The sodium and potassium concentrations of amniotic fluid were also measured. Placental weight was significantly lower in SHR than in WKY between Days 15 and 20 of gestation, but significantly higher on Days 21 and 22. Fetal weight was significantly lower in SHR between Days 17 and 22. These differences were reduced or abolished when fetal and placental weights were corrected for differences in maternal weight between strains. Amniotic fluid volume was significantly lower in SHR between Days 15 and 18, but significantly higher at Days 20, 21 and 22. Amniotic fluid sodium concentration was relatively constant over the period of observation and not different between strains. SHR amniotic fluid potassium concentration was significantly lower than that of WKY near term. Thus, the altered fetal and placental weight of SHR may be due to the overall reduced growth rate of this strain. However, the rate of fluid and electrolyte resorption close to term is markedly different between strains. The mechanism for this altered fluid and electrolyte handling by the SHR feto-placental unit remains to be determined.

Altered uterine environment in the spontaneously hypertensive rat.

1. In order to determine the role of the uterine environment in the development of hypertension in the spontaneously hypertensive rat (SHR) we examined the patterns of fetal and placental growth and the composition of amniotic fluid of SHR and normotensive Wistar-Kyoto (WKY) rats during the final trimester of pregnancy. 2. SHR and WKY embryos and amniotic fluid were collected at days 15 and 20 of pregnancy, and fetal and placental weight and amniotic fluid volume were recorded. The sodium and potassium concentration of amniotic fluid was also measured. 3. Fetal and placental weights were significantly lower in SHR compared to WKY at 15 and 20 days of gestation. Amniotic fluid volume was significantly lower in SHR at 15 days, but significantly higher at 20 days. Amniotic fluid sodium concentration was significantly lower in SHR at 15 days but not different at 20 days when compared to WKY. Potassium concentration was lower in SHR at both ages. 4. Thus the reduced placental weight early in the gestational period of the SHR may play a role in its underdevelopment in utero and hence its reduced birthweight. The SHR foetus is also bathed in a hypokalaemic amniotic fluid of increased volume. How this might influence fetal development and later blood pressure is unclear. Also whether these changes are of maternal or fetal origin remain to be determined.