ABSTRACT
Plane of Nutrition. The plane of nutrition alters the blood level of polyunsaturated fatty acids (mainly arachidonic acid), which are potent stimulators of PG release. These fatty acids can regulate PG production as precursors, as feedback inhibitors (1), or as competitors of arachidonic acid for PG synthase (15); however, other mechanisms of the effect of nutrition on PG release (for example, through nutrition-dependent production of metabolic hormones and growth factors) are not to be excluded (see below). Dietary fatty acids reduced ovarian and endometrial PGF synthesis, decreased ovulation rate in rats, delayed parturition in sheep and humans, and reduced embryonic mortality in cows (15). Pregnancy. Pregnancy dramatically alters the production, metabolism, and effects of PGF and PGE in the uterus. The conceptus produces different substances (interferon-τ in ruminants, estrogen in pigs, see below) that suppress secretion or effects of PGF and activate those of PGE, which, in turn, blocks resorption of the corpus luteum, maternal recognition, and uterine contractility. The start of labor and/or the end of luteal phase of the estrous cycle is associated with the elimination of these effects (1,3-5,17). Menstruation and Inflammation. Menstruation and inflammation are associated with the alteration in ovarian and endometrial production of PGF, PGE, and PGI synthesis, which is induced by the activation of production of endothelin-1, interleukin (IL)-1, tumor necrosis factor (TNF)-α, bradykinin, histamine and related substances; these are potent stimulators of PG release (see below) in these organs (1,4,6,17). Gonadotropin. Gonadotropin effects on PG secretion have not yet been studied extensively, but in our experiments, the exogenous luteinizing hormone (LH) was a potent stimulator of PGF release by cultured bovine granulosa cells (11; Fig. 1).
