Gonadotropin stimulated regulation of the blood-follicle barrier is
mediated by nitric oxide.
Powers, Robert W., Lin Chen, Paul T. Russell, and William J. Larsen.
Developmental Biology and Cell Biology,Neurobiology, and Anatomy,
University of Cincinnati, College of Medicine, and the Center for
Reproductive Studies, Christ Hospital, Cincinnati, Ohio
APStracts 2:0053E, 1995.
While initially described over thirty years ago, the blood-follicle
barrier has remained a biological enigma. In this study, we
characterize the blood-follicle barrier with respect to its
regulation of intrafollicular inter-[alpha]-trypsin inhibitor protein
(I[alpha]I) influx following an ovulatory stimulus. We have found
that I[alpha]I is localized within the ovarian vasculature but is
excluded from the follicular compartment until an ovulatory stimulus.
Within minutes after an ovulatory dose of human chorionic
gonadotropin (hCG), I[alpha]I is localized within the follicular
fluid of responding follicles where this protein becomes associated
with and stabilizes the newly synthesized hyaluronic acid-rich
cumulus extracellular matrix (cECM). Analysis of this process has
shown that intravenous (i.v.) injection of sodium nitroprusside or
excess substrate for nitric oxide synthase, L-arginine, mimics the
effect of gonadotropic hormones on the influx of I[alpha]I into the
follicular compartment of preovulatory follicles. Moreover,
intravenous injection of specific nitric oxide synthase inhibitors,N
-nitro-L-arginine methylester and N-nitro-L-arginine, inhibit
gonadotropin-mediated intrafollicular influx of I[alpha]I and also
inhibit ovulation in the mouse.
Received 1 December 1994; accepted in final form 8 March 1995.
APS Manuscript Number E499-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 4 April 1995.