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[Cation metabolism and the effects of circulating factors in pregnancy induced hypertension]
M Takashima1, H Morikawa, M Yamasaki
1Department of Obstetrics and Gyncology, Kobe University, School of Medicine, Hyogo, Japan.
Insights
Pregnancy induced hypertension (PIH) is linked to increased intracellular calcium and sodium levels in platelets and red blood cells, potentially affecting blood pressure regulation. Serum factors in PIH women may contribute to elevated calcium levels.
Area of Science:
- Biochemistry
- Physiology
- Obstetrics
Context:
- Pregnancy-induced hypertension (PIH) presents complex pathophysiological changes.
- Intracellular ion concentrations, specifically calcium and sodium, are implicated in cardiovascular regulation.
Purpose:
- To investigate the role of intracellular ionized calcium in platelets (p-[Ca2+]i) and ionized sodium in red blood cells (r-[Na+]i) in the pathophysiology of PIH.
- To explore potential serum factors contributing to altered ion levels in PIH.
Summary:
- Measurements in PIH women revealed significantly increased p-[Ca2+]i and r-[Na+]i compared to normal pregnancies.
- Platelet calcium levels increased in PIH, independent of platelet activation, and correlated positively with diastolic blood pressure.
- Incubation with serum from PIH women, 17 beta-estradiol, parathyroid hormone (PTH), or endothelin-1 (ET-1) increased p-[Ca2+]i.
Impact:
- Elevated p-[Ca2+]i and r-[Na+]i in PIH may contribute to increased peripheral vascular resistance and the development/maintenance of hypertension.
- Serum factors in PIH patients appear to play a role in the accumulation of intracellular ionized calcium.
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.