[A study on the membrane Na+ efflux of pregnancy-induced hypertension (PIH)].
In order to elucidate the mechanism of pregnancy-induced hypertension (PIH) from the point of view of vascular resistance, we measured the intracellular Na+ concentrations and the membrane Na+ effluxes using red blood cells from normal pregnant females and patients with PIH. We also discussed the influences of hormones such as estrogen, progesterone, dehydroepiandrosterone sulfate (DHAS), hydrocortisol, human placental lactogen (hPL), human chorionic gonadotropin (hCG), and prolactin and parathyroid hormone (PTH) on the membrane Na+ effluxes. The intracellular Na+ concentrations were lower and the Na+-K+-ATPase activities were slightly higher both in the luteal phase and in the first trimester of normal pregnancy than those in the follicular phase, after which the former gradually increased and the latter gradually decreased until term to the mean values of those in the whole menstrual period. In mild PIH, the intracellular Na+ concentrations were not significantly increased, and the Na+-K+-ATPase activities were significantly increased compared to those in the third trimester of normal pregnancy, which suggests the compensatory increase of the Na+-K+-ATPase activities as opposed to the increase of the intracellular Na+ concentrations. In severe PIH, the intracellular Na+ concentrations were significantly increased compared with those in the third trimester of normal pregnancy and slightly increased compared with those in mild PIH, whereas the Na+-K+-ATPase activities were slightly decreased compared with those in mild PIH, which indicates a breakdown of the compensatory increase of the Na+-K+-ATPase activities. The intracellular Na+ concentrations in PIH are significantly correlated to diastolic pressure, systolic pressure and mean blood pressure. When the male red blood cells were incubated with the hormone, dose-dependently the Na+-K+-ATPase activities were significantly elevated by hydrocortisol and slightly elevated by progesterone and hPL, and they were significantly depressed by estrogen and prolactin and slightly depressed by PTH. These results suggest that the peripheral vascular resistance might be increased in the third trimester of normal pregnancy compared with that in the first trimester because the intracellular Na+ concentrations were elevated, and the Na+-K+-ATPase activities in the cell membrane were decreased along the course of pregnancy as a result of the effects of various hormones in the maternal blood.(ABSTRACT TRUNCATED AT 400 WORDS)
Mimura
O
O
Department of Obstetrics and Gynecology, Kobe University School of Medicine, Japan.
Morikawa
H
H
Yamasaki
M
M
Mochizuki
M
M
D000728:Androgens / Q000502:physiology; D001692:Biological Transport; D002462:Cell Membrane / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism*; D004967:Estrogens / Q000502:physiology; D005260:Female; D006062:Gonadotropins / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology; D006973:Hypertension / Q000209:etiology*; D010281:Parathyroid Hormone / Q000502:physiology; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D012964:Sodium / Q000097:blood*; D014655:Vascular Resistance
D000728:Androgens; D004967:Estrogens; D006062:Gonadotropins; D010281:Parathyroid Hormone; D012964:Sodium; D006854:Hydrocortisone