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Excretion of pregnanetriol during pregnancy
Volume Number
80 5
March, 1960. *Ronan, F. F., Parsons’ L., Namiot, R., and Wotiz, H. H.: Excretion of Pregnanetrio1 During Pregnancy, p. 355. Ronan et al.: Excretion of Pregnanetriol During Pregnancy, p. 355. Evidence is presented that certain enzyme preparations are unable to hydrolyze pregnane-3a, 17a and 2Oa-triol, although they readily cleave pregnane-3a, 20a, diol. Comparison of enzymatic hydrolysis with mineral acid hydrolysis showed that the latter caused conversion of pregnanetriol to a substance with chromatographic properties similar to those of pregnanediol, resulting in interference with the assay of pregnanediol. The excretion of pregnanetriol during pregnancy (7 cases studied) showed two major peaks in the first and third trimesters. Between these peaks there was complete disappearance of pregnanetrio1 from the urine at about the twelfth week. This suggests that the site of production of pregnanetriol precursors had shifted from the ovary and possibly the adrenal cortex to the placenta. J. Edward Hall April, 1960. *Mills, I. H., Scheol, H. P., Chen, P. S., Jr., and Bartter, F. C.: Effect of Estrogen Administration on Metabolism and Protein Binding of Hydrocortisone, p. 515. *Assali, N. S., Dignam, W. J., and Long, L.: Renal Function in Human Pregnancy. III. Effects of ADH on Renal Hemodynamics and Water and Electrolyte Excretion Near Term and Postpartum, p. 581. Mills et al.: Effect of Estrogen Administration on Metabolism and Protein Binding of Hydrocortisone, p. 5 15. A study was made of the effect of estrogen administration on the plasma hydrocortisone level in normal subjects with and without concomitant cortisone therapy. Plasma hydrocortisone levels in some instances fall progressively during the control period with cortisone alone. This is reversed by ultrafiltration at 37O C. and double isotope tracer techniques, the protein-bound and nonprotein-bound fractions of plasma hydrocortisone were studied. Approximately 5 to 10 per cent was not protein bound. This percentage was reduced, but absolute values remained the same, when estrogen was given. The rise in the plasma level of hydrocortisone rep-
Selected
abstracts
1035
resented an increase in the protein-hound fraction, and in vitro techniques revealed an increase in the binding protein or in the number of sites. The increased plasma levels due to estrogen therapy were not associated with depression of eosinophils, which suggests that only the nonprotein-bound fraction is biologically active. The half-time for disappearance of plasma hydrocortisone is considerably prolonged by administration of estrogen, this probably represents protection from destruction by the liver by means of greater protein binding. The effects of estrogen in altering hydrocortisone metabolism are comparable to those produced by pregnancy. J. Edward Hall Assali, Dignam, and Long: Renal Function in Human Pregnancy, p. 581. It has been suggested that pregnant women are less sensitive to the action of ADH because they possess an inactivating mechanism for this hormone. This hypothesis was tested by studying the effects of intravenous administration of Pitressin on renal hemodynamics and water and electrolyte excretion in pregnant women in the latter part of gestation and in postpartum and nonpregnant subjects. During pregnancy, a single intravenous dose of 100 mu. of Pitressin or continuous infusion of this hormone in doses varying from 25 to 100 mu. per hour produced a marked fall in urine flow with a simultaneous fall in renal plasma flow, glomerular filtration rate, and the output of sodium, chloride, and total solute. Potassium excretion was inconsistent. Osmolal and free water clearance fell, the latter becoming negative in most instances. Following delivery or in the nonpregnant state, the same or higher doses of Pitressin produced a reduction in urine Row which was of the same magnitude and pattern as that in the pregnant subjects. However, renal hemodynamics remained unchanged and electrolyte excretion even increased. This response was typical of the action of Pitressin as described in the literature. Although various hypotheses are offered to explain the altered response to Pitressin in pregnancy, at present it is not possible to identify precisely the factors that account for the change in renal hemodynamics and the fall in solute excretion. The results of the present study do not lend support to the hypothesis suggested by others that an inactivating mechanism for ADH exists in human pregnancy. J. Edward Hall
80 5
March, 1960. *Ronan, F. F., Parsons’ L., Namiot, R., and Wotiz, H. H.: Excretion of Pregnanetrio1 During Pregnancy, p. 355. Ronan et al.: Excretion of Pregnanetriol During Pregnancy, p. 355. Evidence is presented that certain enzyme preparations are unable to hydrolyze pregnane-3a, 17a and 2Oa-triol, although they readily cleave pregnane-3a, 20a, diol. Comparison of enzymatic hydrolysis with mineral acid hydrolysis showed that the latter caused conversion of pregnanetriol to a substance with chromatographic properties similar to those of pregnanediol, resulting in interference with the assay of pregnanediol. The excretion of pregnanetriol during pregnancy (7 cases studied) showed two major peaks in the first and third trimesters. Between these peaks there was complete disappearance of pregnanetrio1 from the urine at about the twelfth week. This suggests that the site of production of pregnanetriol precursors had shifted from the ovary and possibly the adrenal cortex to the placenta. J. Edward Hall April, 1960. *Mills, I. H., Scheol, H. P., Chen, P. S., Jr., and Bartter, F. C.: Effect of Estrogen Administration on Metabolism and Protein Binding of Hydrocortisone, p. 515. *Assali, N. S., Dignam, W. J., and Long, L.: Renal Function in Human Pregnancy. III. Effects of ADH on Renal Hemodynamics and Water and Electrolyte Excretion Near Term and Postpartum, p. 581. Mills et al.: Effect of Estrogen Administration on Metabolism and Protein Binding of Hydrocortisone, p. 5 15. A study was made of the effect of estrogen administration on the plasma hydrocortisone level in normal subjects with and without concomitant cortisone therapy. Plasma hydrocortisone levels in some instances fall progressively during the control period with cortisone alone. This is reversed by ultrafiltration at 37O C. and double isotope tracer techniques, the protein-bound and nonprotein-bound fractions of plasma hydrocortisone were studied. Approximately 5 to 10 per cent was not protein bound. This percentage was reduced, but absolute values remained the same, when estrogen was given. The rise in the plasma level of hydrocortisone rep-
Selected
abstracts
1035
resented an increase in the protein-hound fraction, and in vitro techniques revealed an increase in the binding protein or in the number of sites. The increased plasma levels due to estrogen therapy were not associated with depression of eosinophils, which suggests that only the nonprotein-bound fraction is biologically active. The half-time for disappearance of plasma hydrocortisone is considerably prolonged by administration of estrogen, this probably represents protection from destruction by the liver by means of greater protein binding. The effects of estrogen in altering hydrocortisone metabolism are comparable to those produced by pregnancy. J. Edward Hall Assali, Dignam, and Long: Renal Function in Human Pregnancy, p. 581. It has been suggested that pregnant women are less sensitive to the action of ADH because they possess an inactivating mechanism for this hormone. This hypothesis was tested by studying the effects of intravenous administration of Pitressin on renal hemodynamics and water and electrolyte excretion in pregnant women in the latter part of gestation and in postpartum and nonpregnant subjects. During pregnancy, a single intravenous dose of 100 mu. of Pitressin or continuous infusion of this hormone in doses varying from 25 to 100 mu. per hour produced a marked fall in urine flow with a simultaneous fall in renal plasma flow, glomerular filtration rate, and the output of sodium, chloride, and total solute. Potassium excretion was inconsistent. Osmolal and free water clearance fell, the latter becoming negative in most instances. Following delivery or in the nonpregnant state, the same or higher doses of Pitressin produced a reduction in urine Row which was of the same magnitude and pattern as that in the pregnant subjects. However, renal hemodynamics remained unchanged and electrolyte excretion even increased. This response was typical of the action of Pitressin as described in the literature. Although various hypotheses are offered to explain the altered response to Pitressin in pregnancy, at present it is not possible to identify precisely the factors that account for the change in renal hemodynamics and the fall in solute excretion. The results of the present study do not lend support to the hypothesis suggested by others that an inactivating mechanism for ADH exists in human pregnancy. J. Edward Hall