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The Source of Inhibin Secretion during the Human Menstrual Cycle^*

P. J. ILLINGWORTH, K. REDDI, K. B. SMITH and D. T. BAIRD

Department of Obstetrics and Gynaecology, University of Edinburgh and MRC Reproductive Biology Unit, Centre for Reproductive Biology Edinburgh, Scotland

Address correspondence and requests for reprints to: Dr. P. J. Illingworth, Department of Ob/Gyn, University of Edinburgh and MRC Reproductive Biology Unit, Center for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3, 9EW, Scotland.

The source of inhibin secretion during the human menstrual cycle was investigated in two ways. The concentration of inhibin was compared in samples obtained from the ovarian and peripheral veins of 41 women undergoing hysterectomy. In 13 of the women, the corpus luteum was enucleated at operation and the peripheral concentration of inhibin measured at intervals for 24 h. Inhibin was assayed by a heterologous RIA using an antiserum raised against 31 kilodalton bovine inhibin.

The concentrations of estradiol and progesterone in the peripheral and ovarian veins were similar to those previously reported. During the early follicular phase, the geometric mean inhibin concentrations were found to be significantly higher in both the right and left ovarian veins than the peripheral vein (180.4 and 157.7 vs. 78.7 U/L: P < 0.02) but no difference was found in the late follicular phase between the vein draining the dominant ovary and the contralateral ovarian vein (231.1 vs. 193.4 U/L: NS). The inhibin concentrations in the veins draining the ovary bearing a corpus luteum were, however, significantly higher than those in the contralateral ovarian veins during the mid (409.1 vs. 203.6 U/L: P < 0.02) and late (287.1 vs. 153.2 U/L: P < 0.01) luteal phases. After enucleation of the corpus luteum, the inhibin concentration fell from the level seen before lutectomy (134.4 U/L) to 80.0 U/L at 24 h (P < 0.01).

This study demonstrates conclusively that the human corpus luteum secretes inhibin. No increase in inhibin secretion was seen from the dominant follicle in the late follicular phase. This casts doubt on the hypothesis that the selective suppression of FSH during the follicular phase is due to inhibin from the dominant follicle.

^* This work was supported by grants from the Medical Research Council of the United Kingdom (G426375) and the Wellcome Trust.

Wellcome Trust Clinical Training Fellow.

Received March 19, 1990.

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