FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2181983966> ?p ?o ?g. }

• W2181983966 endingPage "323" @default.
• W2181983966 startingPage "263" @default.
• W2181983966 abstract "In many nonprimate mammalian species, cyclical regression of the corpus luteum (luteolysis) is caused by the episodic pulsatile secretion of uterine PGF 2α , which acts either locally on the corpus luteum by a countercurrent mechanism or, in some species, via the systemic circulation. Hysterectomy in these nonprimate species causes maintenance of the corpora lutea, whereas in primates, removal of the uterus does not influence the cyclical regression of the corpus luteum. In several nonprimate species, the episodic pattern of uterine PGF 2α secretion appears to be controlled indirectly by the ovarian steroid hormones estradiol-17β and progesterone. It is proposed that, toward the end of the luteal phase, loss of progesterone action occurs both centrally in the hypothalamus and in the uterus due to the catalytic reduction (downregulation) of progesterone receptors by progesterone. Loss of progesterone action may permit the return of estrogen action, both centrally in the hypothalamus and peripherally in the uterus. Return of central estrogen action appears to cause the hypothalamic oxytocin pulse generator to alter its frequency and produce a series of intermittent episodes of oxytocin secretion. In the uterus, returning estrogen action concomitantly upregulates endometrial oxytocin receptors. The interaction of neurohypophysial oxytocin with oxytocin receptors in the endometrium evokes the secretion of luteolytic pulses of uterine PGF 2α . Thus the uterus can be regarded as a transducer that converts intermittent neural signals from the hypothalamus, in the form of episodic oxytocin secretion, into luteolytic pulses of uterine PGF 2α . In ruminants, portions of a finite store of luteal oxytocin are released synchronously by uterine PGF 2α pulses. Luteal oxytocin in ruminants may thus serve to amplify neural oxytocin signals that are transduced by the uterus into pulses of PGF 2α . Whether such amplification of episodic PGF 2α pulses by luteal oxytocin is a necessary requirement for luteolysis in ruminants remains to be determined. Recently, oxytocin has been reported to be produced by the endometrium and myometrium of the sow, mare, and rat. It is possible that uterine production of oxytocin may act as a supplemental source of oxytocin during luteolysis in these species. In primates, oxytocin and its receptor and PGF 2α and its receptor have been identified in the corpus luteum and/or ovary. Therefore, it is possible that oxytocin signals of ovarian and/or neural origin may be transduced locally at the ovarian level, thus explaining why luteolysis and ovarian cyclicity can proceed in the absence of the uterus in primates. However, it remains to be established whether the intraovarian process of luteolysis is mediated by arachidonic acid and/or its metabolite PGF 2α and whether the central oxytocin pulse generator identified in nonprimate species plays a mediatory role during luteolysis in primates. Regardless of the mechanism, intraovarian luteolysis in primates (progesterone withdrawal) appears to be the primary stimulus for the subsequent production of endometrial prostaglandins associated with menstruation. In contrast, luteolysis in nonprimate species appears to depend on the prior production of endometrial prostaglandins. In primates, uterine prostaglandin production may reflect a vestigial mechanism that has been retained during evolution from an earlier dependence on uterine prostaglandin production for luteolysis." @default.
• W2181983966 created "2016-06-24" @default.
• W2181983966 creator A5009081735 @default.
• W2181983966 creator A5014604993 @default.
• W2181983966 creator A5048829105 @default.
• W2181983966 date "1999-04-01" @default.
• W2181983966 modified "2023-10-11" @default.
• W2181983966 title "Luteolysis: A Neuroendocrine-Mediated Event" @default.
• W2181983966 cites W1173617356 @default.
• W2181983966 cites W138119483 @default.
• W2181983966 cites W1504906938 @default.
• W2181983966 cites W1527662480 @default.
• W2181983966 cites W1530740124 @default.
• W2181983966 cites W1541228389 @default.
• W2181983966 cites W1542479930 @default.
• W2181983966 cites W1543394585 @default.
• W2181983966 cites W1544502281 @default.
• W2181983966 cites W1557147130 @default.
• W2181983966 cites W1558210941 @default.
• W2181983966 cites W1566559214 @default.
• W2181983966 cites W1589415602 @default.
• W2181983966 cites W1610204701 @default.
• W2181983966 cites W1679854349 @default.
• W2181983966 cites W174227169 @default.
• W2181983966 cites W177045913 @default.
• W2181983966 cites W1870986561 @default.
• W2181983966 cites W1908603549 @default.
• W2181983966 cites W1918406217 @default.
• W2181983966 cites W1963644679 @default.
• W2181983966 cites W1964166828 @default.
• W2181983966 cites W1964181010 @default.
• W2181983966 cites W1964686285 @default.
• W2181983966 cites W1964838850 @default.
• W2181983966 cites W1965304685 @default.
• W2181983966 cites W1966001202 @default.
• W2181983966 cites W1966340756 @default.
• W2181983966 cites W1966575109 @default.
• W2181983966 cites W1966888205 @default.
• W2181983966 cites W1967151666 @default.
• W2181983966 cites W1967385667 @default.
• W2181983966 cites W1967663448 @default.
• W2181983966 cites W1967901025 @default.
• W2181983966 cites W1967971455 @default.
• W2181983966 cites W1968049473 @default.
• W2181983966 cites W1968199040 @default.
• W2181983966 cites W1968925001 @default.
• W2181983966 cites W1969157586 @default.
• W2181983966 cites W1969246488 @default.
• W2181983966 cites W1969786471 @default.
• W2181983966 cites W1969914360 @default.
• W2181983966 cites W1970315882 @default.
• W2181983966 cites W1970533159 @default.
• W2181983966 cites W1970730213 @default.
• W2181983966 cites W1970732751 @default.
• W2181983966 cites W1970863500 @default.
• W2181983966 cites W1971260745 @default.
• W2181983966 cites W1971358516 @default.
• W2181983966 cites W1971451280 @default.
• W2181983966 cites W1971545109 @default.
• W2181983966 cites W1972260789 @default.
• W2181983966 cites W1972399583 @default.
• W2181983966 cites W1973308410 @default.
• W2181983966 cites W1973517260 @default.
• W2181983966 cites W1973578858 @default.
• W2181983966 cites W1973644834 @default.
• W2181983966 cites W1974853601 @default.
• W2181983966 cites W1975337826 @default.
• W2181983966 cites W1975442655 @default.
• W2181983966 cites W1976133375 @default.
• W2181983966 cites W1976803203 @default.
• W2181983966 cites W1977127210 @default.
• W2181983966 cites W1978022500 @default.
• W2181983966 cites W1978071581 @default.
• W2181983966 cites W1978136857 @default.
• W2181983966 cites W1978534918 @default.
• W2181983966 cites W1978767615 @default.
• W2181983966 cites W1978850525 @default.
• W2181983966 cites W1979065558 @default.
• W2181983966 cites W1979803030 @default.
• W2181983966 cites W1980166477 @default.
• W2181983966 cites W1980323936 @default.
• W2181983966 cites W1980446082 @default.
• W2181983966 cites W1980719862 @default.
• W2181983966 cites W1980853146 @default.
• W2181983966 cites W1981648296 @default.
• W2181983966 cites W1981750192 @default.
• W2181983966 cites W1981763058 @default.
• W2181983966 cites W1982039293 @default.
• W2181983966 cites W1982414199 @default.
• W2181983966 cites W1982891994 @default.
• W2181983966 cites W1983001210 @default.
• W2181983966 cites W1983479267 @default.
• W2181983966 cites W1983650658 @default.
• W2181983966 cites W1983663034 @default.
• W2181983966 cites W1983830286 @default.
• W2181983966 cites W1983899018 @default.
• W2181983966 cites W1983905135 @default.
• W2181983966 cites W1984709241 @default.

• next