Recently, ketanserin (serotonin receptor antagonist) has been reported to be beneficial in the treatment of preeclampsia. In this study, we investigated the effects of ketanserin on the placental blood flow, fetal weight and placental weight in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). We measured the rats' placental blood flow by monitoring the clearance of hydrogen gas generated by electrolysis. In ketanserin (12, 24, 48 mg/kg)-treated SHR, systolic blood pressure was significantly decreased. The placental blood flow was significantly (p less than 0.05) reduced compared to that before treatment in WKY and SHR. The fetal weight decreased dose dependently in WKY, while in SHR it did not decrease significantly. The placental weight of ketanserin-treated rats decreased compared to that before treatment. These data suggest that ketanserin might have some reducing effects on placental blood flow, fetal weight and placental weight proportional to the dose.
Recently, prostacyclin (PGI2) has been used for the treatment of preeclampsia. In this study, we investigated the effects of PGI2 on placental blood flow (measured with clearance of hydrogen gas generated by electrolysis) in normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The placental blood flow of PGI2-treated SHR (0.25, 0.5 and 1 mg/kg) was significantly (p < 0.05) reduced compared with WKY. These data suggest that PGI2 has a certain reducing effect on placental blood flow in SHR; on the other hand, in WKY, it has an increasing effect depending on the dose.
The effect of nifedipine on placental blood flow was investigated in spontaneously hypertensive rats (SHR) and compared with that in normotensive Wistar Kyoto rats (WKY) by means of the clearance of hydrogen gas generated by electrolysis. The placental blood flow of nifedipine-treated WKY (5,10 and 25 mg/kg) was significantly (p < 0.05) reduced compared with that of WKY control. On the other hand, the placental blood flow of nifedipine-treated SHR did not change compared with that of SHR control. These data suggest that nifedipine has different effects on placental blood flow in SHR and WKY.
FURUHASHI, N., TSUJIEI, M., KIMURA, H., YAJIMA, A., NAGAE, H. and KIMURA, C. Maternal and Fetal Atrial Natriuretic Peptide Levels, Maternal Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Levels in Normal and Preeclamptic Pregnancies. Tohoku J. Exp. Med., 1991, 165 (2), 79-86-To clarify the possible role of elevated atrial natriuretic peptide (ANP) in the pathophysiology of preeclapmsia, we measured ANP, renin activity (PRA), angiotensin II (Ang II), TXB2 (a stable metabolite of TXA2) and 6-keto-PGF1α (a stable end product of PGI2) concentrations in the plasma of 19 normal pregnant women and 35 severe preeclamptic patients at term. Plasma ANP levels in the preeclamptic patients (n=35, 71.5±3.8pg/ml, mean±S.E.) and also umbilical plasma ANP (n=35, 83.0±4.2pg/ml) were significantly (p<0.01) higher than those of normal pregnant women plasma (n=19, 58.7±3.7pg/ml) and umbilical plasma (n=19, 47.6±4.7pg/ml ). There was a significant (p<0.01) positive correlation between maternal ANP levels and fetal ANP levels (n=54, r=0.44). Plasma PRA and 6-keto-PGF1α levels in preeclampsia were significantly (p<0.05) lower than those of normal pregnancy. The ratio of 6-keto-PGF1α/TXB2 in preeclampsia was significantly (p<0.01) lower than that of normal pregnancy as we reported previously. There was no significant correlation between plasma ANP level and plasma PRA, Ang II, plasma TXB2 and 6-keto-PGF1α concentrations. Moreover there was no significant correlation between plasma ANP level and the severity of preeclampsia. These data suggest the possibility of a transplacental crossing of ANP secreted by feto-placental unit, which might be, at least in part, responsible for the high ANP levels observed in preeclampsia. The ANP in preeclampsia is not related directly to hypertension, but it may play a substantial role in the regulation or normalization of blood volume and vascular reactivity.
Recently, nifedipine (Ca antagonist) has been used for the treatment of preeclampsia. In this study, we investigated the effects of nifedipine on the normotensive Wistar Kyoto rat's placental blood flow, fetal weight and placental weight. We measured the rat's placental blood flow using clearance of hydrogen gas generated by electrolysis. The placental blood flow, placental and fetal weights of nifedipine-treated rats (5, 10 and 25 mg/kg) were significantly (p < 0.05) reduced compared with normal pregnant rats. These data suggest that nifedipine might have some reducing effects on placental blood flow, fetal weight and placental weight.
FURUHASHI, N., TSUJIEI, M., KIMURA, H., YAJIMA, A., KIMURA, C. and IDE, Y. Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Concentrations in 139 Preeclamptic Patients. Tohoku J. Exp. Med., 1990, 162 (3), 235 -241-Plasma renin activity, plasma concentratrions of angiotensin 11(AngII), stable metabolites (6-keto-prostaglandin F1α: 6-keto-PGF1α) of prostacyclin (PGI2) and a metabolite (thromboxane B2: TXB2) of thromboxane A2 (TXA2) were measured with radioimmunoassay(RIA) in 107 normal pregnancy (control) and 139 preeclamptic patients in 28-41 gestational weeks. PRA and 6-keto-PGF1α were significantly higher and AngII was slightly higher in preeclampsia than in control, and TXB2 was significantly lower in preeclampsia in control. The ratio of 6-keto-PGF1α/TXB2 was significantly lower in preeclampsia than in control. These data suggest that the changes in the renin-angiotensin system may not be primary alterations in preeclampsia. It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGF1α and TXB2 are less important than the decrease in the ratio of the 6-keto-PGF1α/TXB2.
