Serum level of Endothelin-1 and its regulatory mechanism in pregnancy-induced hypertension.
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The purpose of this study was to clarify the role of endothelin-1 (ET-1) in the pathophysiology of pregnancy induced-hypertension (PIH).<BR>1) Plasma levels of ET-1, which is a potent vasoconstrictor produced by vascular endothelial cells, were determined in normal and hypertensive pregnancy. Plasma concentration of ET-1 in normal pregnant women in the 3rd trimester was 0.81±0.39pg/ml. The value in patients with mild and severe PIH was 1.01±0.34 and 1.67±0.48pg/ml, respectivery ; the latter were significantly higher than those in normal pregnant women, while the former were also higher but not significantly so. There was a signficant correlationship between serum ET-1 levels and systolic and diastolic blood pressure (r=0.489, p<0.001 and r =0.333, p <0.02, respectively).<BR>2) The serum progesterone level in normal pregnant women (126.1±18.2ng/ml) was higher than that in hypertensive subjects (197.5±92.2ng/ml); however the difference was not statistically significant. The serum concentrations of estradiol in normal and hypertensive pregnant women were 19.5±3.0 and 7.32± 1.55ng/ml, respectively. The value in hypertensive subjects was significantly lower than that in normal pregnant women.<BR>3) (i) Treatment of the cultured endothelial cells with 17β-estradiol (10, 100ng/ml) decreased the ET-1 level in culture media, while it increased the intracellular of the peptide. Changes in the intracellular and extracellular concentration of big ET-1, which is a precursor of ET-1, after the same treatment showed similar results as those of ET-1. (ii) Treatment of the cells with progesterone (10, 500ng/ml) resulted in an increase in the extracellular level of ET-1 and a decrease in intracellular concentration. Changes in the intracellular and extracellular concentration of big ET-1 caused by progesterone treatment were also similar to those of ET-1.The concentration of ET-1 in the cultured media was increased by simultaneous application of 17β-estradiol 10ng/ml and progesterone 300ng/ml. However, the intracellular levels of the peptide were not influenced by combined treatment of the two sex steroids. Changes in level of big ET-1 in the cultured media were similar to those of ET-1. These results suggest that, (i) ET-1 may have a pathophysiological role in PIH, (ii) hypertensive pregnant women may have an altered function in secretory mechanisms of ET-1, (iii) hormonal milieu, in women with PIH, higher progesterone and lower estrogens, may partly contribute to the higher serum concentration of ET-1, and (iv) these sex steroids do not affect the mechanism in conversion of big ET-1 into ET-1. [Adv Obster Gynecol 46(2) : 187-195, 1994 (H6.3)]
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