Pathogenesis Of Pregnancy-induced Hypertension Research Articles

Pre-eclampsia: a hypothesis for its pathogenesis.

A hypothesis is presented according to which the pathogenesis of pregnancy-induced hypertension can be attributed to disturbances in renal function caused by the upright posture of the human. In pregnancy, glomerular filtration rate (GFR) and tubular reabsorption, the latter stimulated by aldosterone, are working in high gear. A diminished GFR with continued stimulation of tubular reabsorption would lead to sodium retention. That situation could result, particularly in the primigravida, from the enlarged uterus of late pregnancy exerting pressure on and interfering with venous return, arterial blood flow to kidneys, and/or ability of ureters to transport urine and maintain low pressure in the kidney pelvis. At an early stage, pre-eclampsia can be controlled by bed rest, quite likely by removing dangerous uterine compression. Animal studies are required to test the hypothesis.

A prospective study of circulating prolactin during primigravid pregnancy.

A prospective, cross-sectional study of 164 primigravid patients was conducted to determine the role of prolactin in the pathogenesis of pregnancy induced hypertension. Clinically normal patients had peripheral venous blood sampled from the lateral and recumbent positions monthly in the morning during their last two trimesters in labor and six weeks postpartum. One-third of the patients had 24 hour urine collections. Homologous double antibody radioimmunoassays were performed to determine prolactin levels. The data were analyzed according to pregnancy outcome: pregnancy-induced hypertension or normotensive throughout pregnancy. Acute positional change did not influence prolactin level. Prolactin levels were significantly elevated in the hypertensive outcome group only at 37-39 weeks and were not correlated with sodium excretion. We conclude that circulating prolactin does not play a significant role in pathogenesis of pregnancy-induced hypertension, but perhaps the elevated levels may be reflecting pathophysiologic changes.