The blood clearance rate (BCR) of cortisol was measured in non-pregnant ewes and in pregnant ewes and their intact or bilaterally adrenalectomized fetuses. In pregnant sheep the placental transfer of cortisol in both directions was established. The BCR of cortisol in the non-pregnant sheep was 51.7 +2- 4.9 (S.E.M.) l/h (n = 36) or 1.15 l/h per kg body weight. This was lower than that in the pregnant ewe (97-143 days of gestation) of 76.9 +/- 4.21 l/h (n = 9) or 1.85 l/h per kg. In the intact fetus the BCR was 8.2 +/- 0.26 l/h (n = 10) over the same period of gestation. The percentage of the maternal production rate of cortisol transferred to the fetus was 1.4 +/- 0.11% (n = 9) and the placental transfer from fetus to mother was 19.5 +/- 1.5% (n = 8). The BCR in pregnant ewes bearing bilaterally adrenalectomized fetuses was not significantly different from that of mothers of intact fetuses (58.4 +/- 7.7 l/h; n = 6). The BCR of adrenalectomized fetuses was 8.4 +/- 1.37 l/h (n = 8). The placental transfer of cortisol from mother to fetus was sufficient to account for all the cortisol measured in adrenalectomized fetuses and in intact fetuses of 100-121 days of gestation. However, it accounted for only 37% of the cortisol measured in fetuses of 122-135 days of gestation and 12% or less in fetuses older than 136 days of gestation.
ACTH administration (80 IU/day for 5 days), which produces hypertension and charateristic metabolic effects in sheep (38), has been compared with the effect of intravenous infusion of cortisol (5 mg/h), corticosterone (0.5 mg/h), deoxycorticosterone (50 mug/h), and 11-deoxycortisol (1 mg/h), each given singly for 5 days. Further, a mixture consisting of aldosterone (3 mug/h), cortisol (5 mg/h), deoxycorticosterone (25 mug/h), corticosterone (0.5 mg/h), and 11-deoxycortisol (1 mg/h), was also infused intravenously for 5 days. In another series of experiments, 18-hydroxydeoxycorticosterone (100 mg/h) was also included in the combined-steroid solution. With the exception of 18-hydroxydeoxycorticosterone, which was not measured, the rates of infusionproduced peripheral arterial blood levels of the steroids similiar to those seen with ACTH stimulation. Blood pressure,water intake, urine output, and plasma and urinary electrolytes were measured: individual steroids had little effect on these, but manyof the metabolic changes produced by ATCH (hypokalemia and increased water intake andurine output) were produced by the combined-steroid infusion. However, the combined-steroid infusion failed to induce an increase in blood pressure similiar to that seen inthe ACTH experiments. Thus the findings are against a major role in ACTH hypertension for any steroid used, either singly or in combination. As yet unrecgnized factor/s may be involved in the ACTH-induced hypertension.
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