title: [Cation metabolism and the effects of circulating factors in pregnancy induced hypertension].
abstract: In order to clarify the pathophysiological significance of changes in intracellular ionized calcium and sodium levels in pregnancy induced hypertension (PIH), the intracellular ionized calcium concentration in platelets (p-[Ca2+]i) and the intracellular ionized sodium concentration in red blood cells (r-[Na+]i) were measured simultaneously in PIH women in the third trimester. p-[Ca2+]i in the first trimester showed a slightly greater increase than in the women of normal luteal phase. In the second trimester, p-[Ca2+]i decreased significantly compared to first trimester, and the third trimester and first trimester levels were the same. In women with mild and severe PIH, the levels in both groups were significantly increased compared with that in normal pregnant women. Thus mechanisms not associated with platelet activation were considered as the cause of the increase of p-[Ca2+]i of women with PIH. r-[Na+]i in mild and severe PIH were also significantly increased compared to normal pregnancy. No correlation between p-[Ca2+]i and r-[Na+]i and diastolic blood pressure was observed in normal pregnancy, but a positive correlation was observed in PIH. When the male platelets were incubated with serum from non-pregnant or normal pregnant women, p-[Ca2+]i did not show any significant changes. On the other hand, p-[Ca2+]i was significantly increased after the incubation with serum from PIH women. Moreover, p-[Ca2+]i was significantly increased after the incubation with 17 beta-estradiol, parathyroid hormone (PTH), or endothelin-1 (ET-1). These data suggest that the increase of p-[Ca2+]i and r-[Na+]i in PIH is important in the initiation and maintenance of hypertension by influencing peripheral vascular resistance, and also various factors in the serum of PIH women may contribute to the accumulation of intracellular ionized calcium in patients with PIH.
authors.affiliation: Department of Obstetrics and Gyncology, Kobe University, School of Medicine, Hyogo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takashima
authors.forename: H
authors.initials: H
authors.lastname: Morikawa
authors.forename: M
authors.initials: M
authors.lastname: Yamasaki
authors.forename: M
authors.initials: M
authors.lastname: Mochizuki
mesh_terms: D001792:Blood Platelets / Q000378:metabolism*; D002118:Calcium / Q000097:blood*; D016232:Endothelins / Q000097:blood; D004912:Erythrocytes / Q000378:metabolism*; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D012964:Sodium / Q000097:blood*
chemical_list: D016232:Endothelins; D010281:Parathyroid Hormone; D004958:Estradiol; D012964:Sodium; D002118:Calcium