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This study examined the effect of LH pulses, of similar amplitude and frequency to those found in the luteal phase, on the pattern of hormone secretion and follicle development in GnRH antagonist-suppressed ewes stimulated with exogenous FSH. This experiment was conducted on ewes with ovarian autotransplants in a continuous study. Follicle development was suppressed in 18 ewes by 3 weeks of GnRH antagonist treatment (50 micrograms/kg per 4 days s.c.), and was then stimulated by infusion of ovine (o)FSH (5 micrograms NIADDK-oFSH-16/h i.v.) for 3 days. In addition to FSH, 10 animals received pulses of LH (2.5 micrograms NIADDK-oLH-26 i.v.) every 4 h for the entire period of the FSH infusion. The follicle population was determined by daily ultrasound. Samples of ovarian and jugular venous blood were collected at 4-h intervals over the period of the FSH infusion and there were three periods of intensive blood sampling (15-min intervals for 2.5 h at 24, 48 and 72 h after the start of the FSH infusion) when the steroidogenic capacity of the follicles in all 18 ewes was tested around an LH challenge (2.5 micrograms i.v.). GnRH antagonist treatment resulted in a 57% decrease in FSH concentrations and prevented ovarian follicle development beyond 3 mm in diameter. Infusion of FSH resulted in a 60% increase in FSH concentrations and stimulated the development of large antral follicles and a coincident increase in ovarian androstenedione, inhibin and oestradiol secretion in both experimental groups. In the absence of 4-hourly LH pulses basal steroid secretion was negligible (< 1 ng/min; P < 0.001). Daily LH challenges, however, revealed no difference in the steroidogenic capacity of the follicle population in either experimental group. Similarly, LH pulses had no effect on the growth rate and number of antral follicles stimulated by FSH infusion, or the pattern of ovarian inhibin secretion. In conclusion, these results show that while FSH alone can stimulate the development of ovulatory sized follicles in ewes made hypogonadal with GnRH antagonist, physiological patterns of LH stimulation have no deleterious effects on FSH-stimulated follicle development and are essential for normal steroidogenesis.
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Search for other papers by M. G. S. Alam in
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ABSTRACT
Dairy cows with a variety of clinical conditions were investigated in an attempt to identify the cause(s) of subfertility. Sequential or simultaneous injections of 20 μg gonadotrophin-releasing hormone (GnRH), 1 mg oestradiol benzoate and 0·06 mg ACTH(1–24) into five clinical cases of ovarian follicular cysts, two cases of poor body condition and one case of lameness and into control cows revealed a failure in the LH positive-feedback response to oestradiol in all eight clinical cases, but in only two out of twelve control cows. Two of the clinical cases and the two non-responding control cows had high or rising initial progesterone concentrations which would explain the absence of response. All cows studied responded similarly to GnRH and ACTH(1–24).
It is suggested that hypothalamus-pituitary control of LH release may involve a rate-limiting step (in the oestradiol positive-feedback system) and that lesions at this point result in subfertility in a variety of clinical situations.
J. Endocr. (1987) 113, 167–171
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Introduction
Intercellular communication is effected through the release and action of substances known as paracrine agents. Recent studies are providing increasing evidence that pituitary hormone secretion is under the control of paracrine as well as hypothalamic factors. The individual cell types within the rat anterior pituitary gland appear to be arranged in specific groups and juxtapositions, and this precise organization of cells provides an anatomical basis for an intercellular control system in the pituitary gland. There is good circumstantial evidence for a variety of paracrine interactions within the anterior pituitary gland, although the exact physiological functions of different proposed paracrine agents have yet to be fully elucidated. Many substances have been shown to affect the release of each of the pituitary hormones directly, and there is evidence that some of these are synthesized and released within the anterior pituitary and may therefore act as paracrine agents. Established and
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ABSTRACT
Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin ([Sar1,Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin–angiotensin system within the pituitary gland.
J. Endocr. (1988) 116, 367–371
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ABSTRACT
Stress is known to result in lowered female reproductive efficiency. The objective of this study was to examine how increased pituitary-adrenal activity may influence gonadotrophin release in anoestrous ewes.
Various doses (0·06–1·0 mg) of a synthetic adrenocorticotrophic hormone (ACTH(1–24)) preparation were injected into ewes 30 min or 3 h before an i.v. injection of 500 ng gonadotrophin-releasing hormone (GnRH). The LH response to GnRH given 30 min after ACTH(1–24) was similar to that after GnRH alone, whereas the response 3 h after ACTH(1–24) was significantly lower, irrespective of the dose of ACTH(1–24). At 30 min and 3 h after ACTH(1–24) the concentrations of cortisol exceeded 50 nmol/l compared with baseline values of < 10 nmol/l.
The effect of ACTH(1–24) on oestradiol-induced LH release was also examined. Those ewes receiving 0·8 mg ACTH(1–24) depot and 50 μg oestradiol benzoate simultaneously had a preovulatory-type increase in LH 14–20 h later, similar to when oestradiol benzoate was given alone. None of the ewes receiving an additional 0·8 mg ACTH(1–24) depot 10 h after oestradiol benzoate had increases in LH concentration. The cortisol concentrations in all ewes receiving either one or two injections of ACTH(1–24) were > 35 nmol/l at 10 h after the oestradiol injection. However, concentrations of progesterone increased from 0·9 ± 0·3 (s.e.m.) nmol/l at the time of the second ACTH(1–24) injection to 2·1 ±0·3 nmol/l after 2 h.
In summary, it would appear that the suppressive effect of ACTH(1–24) on LH secretion induced by GnRH or oestradiol in the anoestrous ewe is not dependent on increased plasma concentrations of cortisol.
J. Endocr. (1988) 118, 193–197
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Search for other papers by H Dobson in
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Abstract
The present study was designed to investigate whether transport, a mild environmental stressor, could affect the oestradiol-induced LH surge in postpartum ewes and, if so, the mechanism involved. Welsh Mountain ewes, with lambs removed at parturition (day 0) and hand-milked 12 and 48 h later, were given 50 μg oestradiol benzoate intramuscularly at various times postpartum. Blood samples were taken via an indwelling jugular venous catheter every 2 h from 8 to 24 h after oestradiol injection. All results are given as means ± s.d. On day 1 oestradiol was unable to induce an LH surge in any ewe. Transport (10–14 h after oestradiol) delayed the onset of the oestradiol-induced LH surge on day 14 (17·5 ±1·7 vs 14·4±2·0 h, n=5 each; P<0·05), but not on day 28 (14·9 ±2·0 vs 14·0 ±2·4 h, n=5 out of 7). Transport had no effect on the amplitude of the surge on either day. Naloxone treatment (1 mg/kg per 2 h) was unable to prevent the delay caused by transport (18·0±1·1 vs 17·5 ± 1·7 h, n=8 each), and did not affect the amplitude of the surge (28·4±5·3 vs 28·1 ±2·3 ng/ml, n=8 each). The duration of the LH surges were not assessed. On day 7, transport from 16 to 20 h after oestradiol delayed the LH surge (22·8 ±2·0 vs 18·0 ± 2·8 h, n=8 each; P<0·05) and reduced the surge amplitude (19·7 ±1·7 vs 22·8 ±2·8 ng/ml; P<0·05), whilst transport from 10 to 14 h did not. Transport (16 to 20 h) had no effect on surge duration (6·25 ±0·7 vs 6·75 ± 1·0 h). In conclusion, transport inhibited the oestradiol-induced LH release in the early postpartum ewe by a non-opioidergic mechanism, but only if the stressor occurred within 2–3 h of the expected onset of the surge.
Journal of Endocrinology (1994) 142, 447–451
