Secretion of Oxytocin by the Corpus Luteum and its Role in Luteolysis in the Sheep

Sheldrick, E. L.; Flint, A. P. F.

doi:10.1007/978-1-4899-1971-7_17

Cited by 3 publications

(2 citation statements)

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“…However, no confirmation has yet been provided that these immunization procedures do in fact block the effects, or the biological activity, of oxytocin. Sheldrick and Flint (1987) presented evidence to suggest that overstimulation with oxytocin lead to down-regulation, lack of response to exogenous oxytocin and increased estrous cycle length. An increase in hormonal half-life following immunization against gonadotrophins was demonstrated by Cole (1973).…”

Section: Role Of Oxytocinmentioning

confidence: 99%

“…The major secretory product of the CL is progesterone although other peptide and protein hormones such as oxytocin (Sheldrick and Flint, 1987) and relaxin (Anderson, 1987), synthesized and released from the CL of several species, may play important roles in the control of reproductive function. For instance, it has been suggested that luteal oxytocin release in the ewe may play a role in the control of estrous cycle length (Sheldrick and Flint, 1987). More consideration will be given for and against this hypothesis in later sections.…”

Section: Review Of the Literature Introductionmentioning

confidence: 99%

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Aspects of luteal function in pigs and sheep

Conley¹

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Previous studies have demonstrated that estradiol-17p (E2) locally increases corpus luteum (CL) wt in pigs, suggesting a direct luteotropiceffect. This study examined the effect of intraluteal Eg implants on utero-ovarian vein (UOV) progesterone (P4), E2, PGF2a and CL wt in cyclic gilts. Eight gilts were laparotomized on day II (day 0 = first day of estrus), catheters were placed in both UOV and gilts were then divided into 2 equal groups (E2-treated and controls). Each CL on one ovary of E2-treated gilts was injected with a quick curing silastic implant containing E2 while each CL on the contralateral ovary received a vehicle implant. Control gilts received bilateral vehicle implants. Blood was collected at 10 min intervals for 1 hour beginning at 0600 and 1800 h from day 11 today 18. Gilts were ovariectomized on day 19. Corpora lutea were weighed, homogenized and assayed for P4. Utero-ovarian venous plasma was assayed for P4, E2, and PGF2a by validated RIA. No side differences were observed in CL wt or UOV P4 within groups. CL were maintained in E2-treated, but not control gilts as evidenced byCLwt{333 ± 20vs 154 ± 12mg),CLP4content(21.8 ± 2.1 vs.3 ± .1g), and CL P4 concentration (65.7 ± 5.5 vs 2.3 ± .6ng/mg), respectively. Uteroovarian venous P4 values were similar between groups up to 1800 h on d 15, declining from 346 ± 122ng/ml at 1800 hour on day 11 to 147 ± 20ng/ml on day 12, then remaining constant to 1800 hour on day 15. Thereafter UOV P4in E2treated gilts returned progressively today 11 values by 1800 hour on day 18 (364 ± 97ng/ml) while values of control gilts declined to low levels (5.4 ± .6ng/ml). In E2-treated gilts in UOV plasma E2 was elevated 13 fold ipsilateral, and 4 fold contralateral, to the E2-treated ovary in comparison to levels in control gilts. Uterine PGF2a release was suppressed in E2-treated compared to control gilts. E2 (yg quantities) failed to prevent the initial decline in UOV P4 between day 11 and day 15, but subsequently returned CL function to normal, as evidenced by increasing UOV P4, through day 18.

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Section: Role Of Oxytocinmentioning

confidence: 99%