Toxemia of pregnancy and eclampsia.
The various phenomena of toxemia of pregnancy both in primiparous and multiparous women may be explained by postulating a defect in the calcium transport mechanism, both in the smooth muscle of the uterus and vascular smooth muscle as well as a similar defect in platelets. The involvement of prostaglandin E has not been proven to be a factor in human beings but could conceivably play an auxiliary role. Amelioration of the process by delivery would be due to dereased demand for the synthesis of the critical smooth muscle protein or proteins involved in calcium binding and transport because of uterine devolution. Eclampsia would be analogous to hypertensive encephalopathy and represent an acceleration of this process, particularly in the untreated woman.
D000804:Angiotensin II / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D004461:Eclampsia / Q000209:etiology; D005260:Female; D006801:Humans; D009124:Muscle Proteins / Q000096:biosynthesis; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000209:etiology* / Q000503:physiopathology; D011247:Pregnancy; D014599:Uterus / Q000503:physiopathology
D009124:Muscle Proteins; D000804:Angiotensin II; D002118:Calcium