Pulsatile administration of gonadotropin-releasing hormone agonist to gilts actively immunized against gonadotropin-releasing hormone

Sexually mature gilts (n = 20) were actively immunized against GnRH. Primary and booster immunizations of GnRH conjugated to bovine serum albumin induced production of antibodies in all gilts. Nineteen of the gilts became acyclic with suppressed concentrations of gonadotropins and estradiol. Intravenous challenges with 100 micrograms GnRH and 5 micrograms D-(Ala6, des-Gly-NH2(10)) ethylamide GnRH (a GnRH agonist that did not cross-react with antibodies produced by the gilts) caused release of LH and FSH, indicating maintenance of secretory capacity of pituitary gonadotropes in the immunized animals. Gilts were given 100 ng GnRH agonist at 2-h intervals for 72 h (n = 4) or 144 h (n = 10) or did not receive agonist (n = 5). Blood samples were taken every 6 h, and detectable concentrations of LH were observed in 42% and 52% of samples taken from gilts treated with or without agonist. In contrast, serum concentrations of FSH and estradiol were undetectable. Reproductive tracts and anterior pituitaries were taken from gilts at the conclusion of pulsatile administration of GnRH agonist or at 144 h for controls. Pituitary concentration of LH and FSH, uterine wet and dry weight, and size of the uterus were similar among groups. Paired ovarian weights for treated gilts pulsed with GnRH agonist for 72 h were heavier (P less than .05); however, ovaries from all immunized gilts were atrophied without follicular structures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Induction of ovulation in anestrous mares with pulsatile administration of gonadotropin-releasing hormone

Four seasonally anestrous mares (Standardbred), housed under a nonstimulatory photoperiod of 8 hours light:16 hours dark, were administered gonadotropin-releasing hormone (GnRH) in a pulsatile pattern (50 or 250 micrograms of GnRH/hour) for 8 to 18 days during February and March 1985. Treatment with GnRH, irrespective of dose or month, induced an increase in serum luteinizing hormone from a mean pretreatment value typical of anestrus (0.58 +/- 0.02 ng/ml +/- SE) to 10.84 +/- 1.27 ng/ml on day 8 of GnRH treatment. Ovulation in the 4 mares occurred 8.8 +/- 0.7 days after the initiation of pulsatile GnRH administration. In each instance, ovulation was followed by a functional corpus luteum, as indicated by a luteal phase (defined as the number of days on which serum levels of progesterone were greater than 1.0 ng/ml) which lasted 14.5 +/- 0.6 days. These results indicate that infusion of GnRH in a pulsatile pattern is effective in inducing follicular development and ovulation in anestrous mares in the absence of a stimulatory photoperiod.     

Influence of an agonist of gonadotropin-releasing hormone (buserelin) on estrus synchronization and fertility in beef cows.

The objective of this experiment was to determine the effect of sequential treatment with buserelin (a GnRH agonist) and cloprostenol (a prostaglandin F2 alpha analog) on estrous response and fertility in beef cattle with different ovarian conditions. On d 0 (1st d of treatment), the control group (n = 52, 10 heifers and 42 cows) and the GnRH group (n = 48, 10 heifers and 38 cows) received 2 mL of saline or 2 mL of Receptal (8 micrograms of buserelin), respectively. On d 6, all cows that had not exhibited spontaneous estrus were given i.m. 500 micrograms of cloprostenol (PGF). Ultrasonography on d 0 and assays of progesterone in blood on d -11, 0, and 6 were used to identify follicular and luteal status of animals. Cattle were observed for estrus from d 0 to 10. Cows showing estrus were bred artificially 12 h after onset of estrus. Over the 10-d period, the number of cows detected in estrus and pregnancy and conception rates were identical for the two groups. However, between d 0 and 6, the proportion of cows exhibiting estrus was lower (P less than .01) in the GnRH group than in the control group. Between d 6 and 10, the synchronization rate and precision of estrus were greater (P less than .01) in the buserelin-treated group than in the control group. Conception rate and interval from PGF injection to onset of estrus were not different between the two treatment groups. Presence of a large (greater than 10 mm) follicle on d 0 enhanced synchronization rate and precision of estrus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of gonadotropin-releasing hormone for hastening ovulation in transitional mares

Natural GnRH and its analog have potential for hastening ovulation in mares. A study was conducted to evaluate the efficacy of a GnRH agonist given either as an injectable or s.c. implant for induction of ovulation in mares. Forty-five seasonally anestrous mares (March) were assigned to one of three groups (n = 15/group): 1) untreated controls; 2) i.m. injection of the GnRH agonist buserelin at 12-h intervals (40 micrograms/injection for 28 d or until ovulation) and 3) GnRH agonist administered as a s.c. implant (approximately 100 micrograms/24 h for 28 d). Six mares per group were bled on d 0, 7, 14 and 21 after injection or insertion of implant. Samples were taken at -1, -.5 and 0 h and at .5, 1, 1.5, 2, 4, 6 and 8 h after GnRH. Additional daily samples were drawn for 28 d after injection or until ovulation. Samples were assayed for concentration of LH and FSH. Progesterone concentrations were determined in samples collected on d 4, 6 and 10 after ovulation. Number and size of follicles and detection of ovulation were determined by ultrasonography. Number of mares induced to ovulate within 30 d was 0 of 15, 7 of 15 and 9 of 15 for groups 1, 2 and 3, respectively. During treatment, follicle sizes were smaller for mares in group 3 (implant). The LH response to GnRH agonist (area under curve) was similar among groups at d 0 but was greater (P less than .05) for mares in group 3 on d 7 and 14 and groups 2 and 3 on d 21 than for controls. A similar pattern was detected for peak concentrations of LH after GnRH on d 0, 7, 14 and 21. Daily concentrations of LH remained low in untreated control mares compared with GnRH-treated mares throughout the sampling period. Concentrations of LH for mares in group 3 that ovulated were elevated greatly above those for group 2 mares, whereas concentrations of FSH were similar in both treatment groups prior to ovulation.     

Detection of urinary luteinizing hormone in Japanese black cows after administration of gonadotropin-releasing hormone

The blood luteinizing hormone (LH) surge in cows is well studied. However, little is known about urinary LH in cows. This study examined urinary LH concentrations after administration of gonadotropin-releasing hormone (GnRH) in six Japanese black cows to induce LH secretion from the pituitary gland into the bloodstream. Abrupt rises in plasma and urinary LH were observed after GnRH administration. Plasma and urinary LH peaked at 2 and 5 hr, respectively. A positive correlation was observed between plasma LH concentrations and urinary LH amounts. Ovulation was confirmed in the cows after 48 hr of GnRH administration. These data strongly suggest that urinary LH is derived from plasma LH, which triggers ovulation in cows.     

Responses of seasonally anovulatory mares to daily administration of thyrotropin-releasing hormone and(or) gonadotropin-releasing hormone analog

Seventeen seasonally anovulatory light horse mares were treated daily, starting January 5 (d 1), for 28 d with GnRH analog (GnRH-A; 50 ng/kg BW) and(or) thyrotropin-releasing hormone (TRH; 5 microg/kg BW) in a 2 x 2 factorial arrangement of treatments to test the hypothesis that combined treatment may stimulate follicular growth and development. Ovaries were examined via ultrasonography and jugular blood samples were collected every 3 d. Frequent blood samples were collected after treatment injections on d 1, 2, 4, 7, 11, 16, and 22; on d 29, all mares received an i.v. mixture of GnRH, TRH, sulpiride, and EP51389 (a growth hormone secretagogue) to assess pituitary responsiveness. No consistent effects (P > 0.1) of treatment were observed for plasma LH, FSH, prolactin, or thyroxine concentrations in samples collected every 3 d. The only effect on ovarian follicle numbers was a reduction in number of follicles 11 to 19 mm in diameter due to TRH treatment (P = 0.029). No mare ovulated during treatment. On the days of frequent sampling, mean LH (P = 0.0001) and FSH (P = 0.001) concentrations were higher in mares receiving GnRH-A and tended to increase from d 1 through 7. In contrast, mean prolactin (P = 0.001) and thyroid-stimulating hormone (P = 0.0001) concentrations were high in mares receiving TRH on d 1 but rapidly decreased thereafter. When mares were administered the secretagogue mixture on d 29, the LH response was greater (P = 0.0002) in mares that had previously received GnRH-A but the FSH response was not affected (P > 0.1); the prolactin response was greater (P = 0.014) and the TSH response was smaller (P = 0.0005) in mares that had previously received TRH. Surprisingly, an immediate growth hormone response to EP51389 was absent in all mares. In conclusion, daily GnRH-A treatment stimulated plasma LH and FSH concentrations immediately after injection; although no long-term elevation in preinjection concentrations was achieved, the responses gradually increased over time, indicating a stimulation of gonadotropin production and storage. Daily treatment with TRH stimulated plasma TSH and prolactin concentrations, but the response diminished rapidly and was minimal within a few days, indicating a depletion of pituitary stores and little or no stimulation of production. There was no beneficial effect of adding TRH treatment to the daily GnRH-A regimen.     

Effects of a gonadotropin-releasing hormone antagonist and altrenogest on luteinizing hormone concentration and ovulation in the mare

The objective of Experiment 1 was to determine a dose and frequency of gonadotropin-releasing hormone (GnRH) antagonist administration to effectively suppress serum luteinizing hormone (LH) concentration and to delay ovulation when administered to mares. The objectives of Experiment 2 were 1) to determine the effects of subcutaneous or intravenous administration of a GnRH antagonist or oral altrenogest on serum LH concentration in the estrual mare; and 2) to determine the effectiveness of human chorionic gonadotropin (hCG) in inducing ovulation in mares with suppressed LH concentrations. In Experiment 1, mares (N = 20) were randomly assigned and treated with either 5% mannitol (control, single subcutaneous injection, 1 mL, at time 0; n = 5); low-dose GnRH antagonist (single subcutaneous injection, 0.01 mg/kg, at time 0; n = 5); frequent low-dose GnRH antagonist (subcutaneous injections, 0.01 mg/kg, at 0, 6, 18, and 24 hours; n = 5); or high-dose GnRH antagonist (single subcutaneous injection, 0.04 mg/kg, at time 0; n = 5). Both the frequent low-dose and high-dose GnRH antagonist treatments resulted in significantly lower LH concentrations compared with controls at 90, 102, and 114 hours after treatment (P < .05). In Experiment 2, mares (N = 38) were randomly assigned and treated with subcutaneous sterile saline (control), altrenogest (oral), subcutaneous GnRH antagonist, or intravenous GnRH antagonist. LH concentration for the altrenogest group was lower than the control group at 3, 4, 18, and 30 hours after treatment (P < .05). LH concentration for both the subcutaneous and intravenous GnRH antagonist groups were lower compared with the control group at several time points (P < .05). Based on these data, dose but not frequency of administration of a GnRH antagonist lowered LH concentration in the estrous mare but did not delay ovulation. In addition, serum LH concentrations can be lowered and ovulation effectively postponed in mares treated with altrenogest followed by administration of hCG. This indicates that serum LH concentrations can be lowered and ovulation effectively postponed in mares treated with altrenogest followed by administration of hCG.     

Fixed-time artificial insemination in replacement beef heifers after estrus synchronization with human chorionic gonadotropin or gonadotropin-releasing hormone

We determined the effects of hCG on ovarian response, concentration of progesterone, and fertility in a fixed-time AI (TAI) protocol. Four hundred forty-four crossbred beef heifers were synchronized with the CO-Synch + CIDR (controlled internal drug-releasing insert) protocol. In addition, heifers were randomly assigned to 1 of 4 treatments in a 2 × 2 factorial arrangement of treatments with main factors being 1) pretreatment, no treatment (control), or treatment with 1,000 IU of hCG 14 d before the initiation of the CO-Synch + CIDR protocol and 2) treatment, administration of 1,000 IU of hCG or 100 μg of GnRH at CIDR insertion of the CO-Synch + CIDR protocol. Blood samples were collected from all heifers on d -21, -14, -7, 0, and 2 relative to PGF(2α) injection. Transrectal ultrasonography was used to examine ovaries in a subset of heifers (n = 362) on d -7 and 0 relative to PGF(2α), and to determine pregnancy status of all heifers on d 33 and 82 relative to AI. Pregnancy rates were similar for heifers pretreated with control (33.0%) or hCG (36.4%), whereas pregnancy rates were greater (P < 0.01) for heifers treated with GnRH (40.1%) compared with hCG (29.0%) at CIDR insertion. Heifers pretreated with hCG had more (P < 0.01) corpora lutea present on the day of CIDR insertion and the day of CIDR removal compared with untreated heifers. A greater proportion (P < 0.01) of heifers ovulated as a result of administration of hCG at the time of CIDR insertion (59.0%) compared with GnRH (38.7%). Heifers treated with hCG at CIDR insertion had greater (P < 0.01) concentrations of progesterone compared with those receiving GnRH at the time of CIDR removal (2.42 ± 0.13 vs. 1.74 ± 0.13 ng/mL; P < 0.01) and at fixed-time AI (0.52 ± 0.03 vs. 0.39 ± 0.03 ng/mL; P < 0.01). Therefore, hCG was more effective than GnRH in its ability to ovulate follicles and to increase concentrations of progesterone in beef heifers. Presynchronization with hCG 14 d before CIDR insertion did not alter pregnancy rates, whereas replacing GnRH with hCG at CIDR insertion decreased pregnancy rates.     

Progesterone concentration,estradiol pretreatment,and dose of gonadotropin-releasing hormone affect gonadotropin-releasing hormone-mediated luteinizing hormone release in beef heifers

We examined whether progesterone (P₄)-induced suppression of LH release in cattle can be overcome by an increased dose of exogenous gonadotropin-releasing hormone (GnRH) or pretreatment with estradiol (E₂). In Experiment 1, postpubertal Angus-cross heifers (N = 32) had their 2 largest ovarian follicles ablated 5 d after ovulation. Concurrently, these heifers were all given a once-used, intravaginal P₄-releasing insert (CIDR), and they were randomly assigned to be given either prostaglandin F_2α (Low-P₄) or no treatment (High-P₄) at follicle ablation, and 12 h later. Six days after emergence of a new follicular wave, half of the heifers in each group (n = 8) were given either 100 or 200 μg of GnRH i.m. Plasma luteinizing hormone (LH) concentrations were higher in the Low- vs High-P₄ groups, and in heifers given 200 vs 100 μg of GnRH (mean ± SEM 15.4 ± 2.2 vs 9.1 ± 1.2, and 14.8 ± 2.1 vs 9.8 ± 1.4 ng/mL, respectively; P ≤ 0.01). Ovulation rate was higher (P = 0.002) in the Low-P₄ group (15/16) than in the High-P₄ group (6/16), but it was not affected by GnRH dose (P = 0.4). In Experiment 2, heifers (n = 22) were treated similarly, except that 5.5 d after wave emergence, half of the heifers in each group were further allocated to be given either 0.25 mg estradiol benzoate i.m. or no treatment, and 8 h later, all heifers were given 100 μg GnRH i.m. Both groups treated with E₂ (Low- and High-P₄) and the Low-P₄ group without E₂ had higher peak plasma LH concentrations compared to the group with high P₄ without E₂ (12.6 ± 1.8, 10.4 ± 1.8, 8.7 ± 1.3, and 3.9 ± 1.2 ng/mL, respectively; (P < 0.04)). However, E₂ pretreatment did not increase ovulation rates in response to GnRH (P = 0.6). In summary, the hypotheses that higher doses of GnRH will be more efficacious in inducing LH release and that exogenous E₂ will increase LH release following treatment with GnRH were supported, but neither significantly increased ovulation rate.     

Administration of human chorionic gonadotropin to suckled beef cows before ovulation synchronization and fixed-time insemination: replacement of gonadotropin-releasing hormone with human chorionic gonadotropin

Two experiments were conducted to evaluate whether hCG administered 7 d before initiating the CO-Synch + controlled internal drug release (CIDR) ovulation synchronization protocol (Exp. 1 and 2), or replacing GnRH with hCG at the time of AI (Exp. 1), would improve fertility to a fixed-time AI (TAI) in suckled beef cows. In addition, the effects of hCG on follicle dynamics, corpus luteum development, and concentrations of progesterone (P4) were evaluated. In Exp. 1, cows were stratified by days postpartum, age, and parity and assigned randomly to a 2 × 2 factorial arrangement of 4 treatments: 1) cows received 100 μg of GnRH at CIDR insertion (d -7) and 25 mg of PGF(2α) at CIDR removal (d 0), followed in 64 to 68 h by a TAI plus a second injection of GnRH at TAI (CG; n = 29); 2) same as CG but the second injection of GnRH at the time of insemination was replaced by hCG (CH; n = 28); 3) same as CG, but cows received hCG 7 d (d -14) before CIDR insertion (HG; n = 28); and 4) same as HG, but cows received hCG 7 d (d -14) before CIDR insertion (HH; n = 29). Pregnancy rates were 52, 41, 59, and 38% for GG, GH, HG, and HH, respectively. Cows receiving hCG (39%) in place of GnRH at TAI tended (P = 0.06) to have poorer pregnancy rates than those receiving GnRH (56%). Pre-CO-Synch hCG treatment increased (P < 0.05) the percentage of cows with concentrations of P4 >1 ng/mL at d -7, increased (P < 0.02) concentration of P4 on d -7, and decreased (P < 0.001) the size of the dominant follicle on d 0 and 3, compared with cows not treated with hCG on d -14. In Exp. 2, cows were stratified based on days postpartum, BCS, breed type, and calf sex and then assigned to the CG (n = 102) or HG (n = 103) treatments. Overall pregnancy rates were 51%, but no differences in pregnancy rates were detected between treatments. Pre-CO-Synch hCG treatment increased (P < 0.05) the percentage of cows cycling on d -7 and increased (P < 0.05) concentrations of P4 on d -7 compared with pre-CO-Synch controls. Therefore, pretreatment induction of ovulation after hCG injection 7 d before initiation of CO-Synch + CIDR protocol failed to enhance pregnancy rates, but replacing GnRH with hCG at the time of AI may reduce pregnancy rates.     

Luteinizing hormone (LH) response to different doses of synthetic gonadotropin releasing hormone (GnRH) in prepubertal gilts

The object of this investigation was to study luteinizing hormone (LH) response to different doses of synthetic gonadotropin-releasing hormone (GnRH) in prepubertal gilts. Four crossbred prepubertal gilts, 128–134 days old and body weight 57–63 kg, were used in this study. Four doses, 0. 5, 25 and 125 μg, of GnRH were administered via a jugular vein catheter in a latin square design. Each treatment consisted of 3 injections at 90 min intervals. Frequent blood samples were taken during a period of 90 min before up to 90 min after treatment. Total LH responses were measured from post-treatment samples as the area under the curve above base level obtained from pre-treatment samples. A positive relationship between GnRH dose and LH release was obtained in all gilts, except for 1 treatment given to a gilt with high plasma level of oestradiol-17β on the day of treatment. This study has demonstrated the responsiveness of the pituitary gland by LH release to different doses of GnRH in 4.5-month-old prepubertal gilts.     

Luteinizing hormone and progesterone concentrations and induction of estrus after use of norgestomet ear implants or constant infusion of gonadotropin-releasing hormone in anestrous, nonlactating dairy goats

Plasma luteinizing hormone and progesterone concentrations, time to onset of estrus, and pregnancy rates were determined in nonlactating anestrous does given 1 of 4 treatments: subcutaneous ear implants containing 3 mg of norgestomet for 9 days (NOR; n = 6); subcutaneous administration, using osmotic minipumps, of 250 ng of gonadotropin-releasing hormone (GnRH)/h for 48 hours (GnRH; n = 6); 3 mg of NOR for 9 days, followed immediately by 250 ng of GnRH/h for 48 hours (NOR + GnRH; n = 6); or no treatment (control; n = 6). During the 72-hour period after removal of NOR or insertion of GnRH pumps, 6 of 6, 0 of 6, 6 of 6, and 3 of 6 does were observed in estrus at a mean (+/- 13.8) hours in groups NOR, GnRH, NOR + GnRH, and control, respectively. Time from end of treatment to peak concentrations of luteinizing hormone were 56 +/- 4.0, 28 +/- 4.7, 34 +/- 4.3, and 41 +/- 9.7 hours (mean +/- SE) for NOR, GnRH, NOR +/- GnRH, and control, respectively. Peak concentrations of luteinizing hormone were significantly greater and occurred significantly later in does given NOR. Progesterone concentrations in does that became pregnant increased to concentrations greater than or equal to 1.0 ng/ml 3 to 5 days after breeding and remained high. Functional corpora lutea (CL) was found in 6 does that did not become pregnant, 1 CL was associated with pseudopregnancy and 1 CL was associated with ovulation prior to placement of the GnRH pumps. Functional CL failed to form in 10 of the 12 doses in groups GnRH and control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of chronic gonadotropin-releasing hormone agonist treatment on serum luteinizing hormone and testosterone concentrations in boars.

Mature boars were subjected to chronic treatment with a gonadotropin-releasing hormone (GnRH) agonist, goserelin (D-Ser[But]6, Azgly-NH210), and serum luteinizing hormone (LH) and testosterone concentrations were measured. Ten sexually mature boars were randomly assigned to treatment (n = 5) or control (n = 5) groups. On day 0, boars were implanted sc (day 0) with 2 GnRH agonist implants (1 mg of GnRH/implant) or sham implants. Blood samples were collected at 12-hour intervals on days -2 and -1, at 6-hour intervals on days 0 through 4, and at 12-hour intervals on days 5 through 8. In addition, blood samples were collected at 15-minute intervals for 6 hours on days -1, 0, 4, and 8. Serum testosterone and LH concentrations were determined by radioimmunoassay. Maximal LH (7 +/- 1 ng/ml) and testosterone (26 +/- 3 ng/ml) concentrations were observed at 5 and 18 hours, respectively, after GnRH agonist treatment. Subsequently, LH and testosterone concentrations decreased to pretreatment values (0.3 +/- 0.1 ng/ml and 1.8 +/- 0.4 ng/ml, respectively) by 24 and 48 hours, respectively, after GnRH agonist implantation. Few differences in the characteristics of pulsatile LH release were observed between the groups. Testosterone and LH concentrations in samples collected at 6- and 12-hour intervals and pulsatile LH release did not change after sham treatment of control boars. Whereas previous reports indicated that chronic GnRH administration suppressed serum LH and testosterone concentrations in rams, rats, and dogs, our results indicate that chronic GnRH agonist treatment induced transitory increases, without subsequent suppression, in LH and testosterone concentrations in mature boars.     

Steroid hormone levels in follicular fluid of swine with spontaneous estrus and ovulation synchronization

The steroid hormones oestradiol 17 beta, oestrone (E1), testosterone (T), and progesterone (P) were quantitatively determined in follicular fluids in the pre-oestric phase of pigs with spontaneous oestrus and synchronised ovulation. As a whole, mean steroid hormone concentrations exhibited characteristic curves in spite of a relatively wide scatter of individual values. Drastic decline in oestrogen concentration in pigs with spontaneous oestrus and synchronised ovulation was accompanied by rise of P levels, while T values stayed relatively constant. As compared to spontaneous oestrus, treatment for synchronised ovulation caused significantly higher increases in follicular T levels. Positive (P) or negative (E1, T) correlations were found to exist between follicle size and steroid hormone concentration. Conclusions are suggested for further studies.     

Induction of ovulation in the prepuberal gilt by pulsatile administration of gonadotropin releasing hormone

An attempt was made to induce precocious puberty in gilts approximately 164 days of age by stimulating a luteinizing hormone (LH) secretory pattern similar to that which occurs before normal onset of puberty. Hourly iv administration of 1 μg synthetic gonadotropin releasing hormone (GnRH) for 7 or 8 days resulted in a mean serum LH concentration of 1.7 ± .3 ng/ml in three treated gilts compared with .9 ± .1 ng/ml in three control gilts (P<.08). Serum LH peak frequency was also greater (P<.05) in treated (3.4 ± .5 peaks/4 hr) than in control gilts (1.2 ± .1 peaks/4 hr), but serum LH peak amplitude was not altered (P>.33) by GnRH treatment. All treated gilts displayed estrus and ovulated within 6 days after treatment began, and all control gilts remained prepuberal throughout the study (P=.05). Only one of the three treated gilts displayed a normal estrous cycle and reovulated after treatment. Precocious ovulation but not puberty was induced in gilts by hourly administration of 1 μg synthetic GnRH, indicating that the pituitary and ovaries of 164-day-old gilts are competent and that final sexual maturation occurs at the hypothalamic level.     

Oral administration of peptidergic growth hormone (GH) secretagogue KP102 stimulates GH release in goats

To assess the oral activity of KP102 (also known GHRP-2) on growth hormone (GH) release in ruminant animals, 5 or 10 mg/kg body weight (BW) of KP102 dissolved in saline was orally administered twice at 2 hr-intervals to either 1- or 3-mo-old goats (n = 5-6). Plasma GH concentrations in the 1-mo-old goats were elevated at 15 min after the first administration of both 5 and 10 mg/kg BW of KP102. Significant elevation of GH concentrations continued until 180 min after 10 mg/kg BW of KP102, whereas the elevated GH levels after the administrations of 5 mg/kg BW of KP102 subsided to basal concentrations within 90 min. The second administration of 10 mg/kg BW of KP102 failed to elevate the GH concentration, but 5 mg/kg BW of KP102 abruptly stimulated GH release. Plasma GH concentrations in the 3-mo-old goats were also significantly elevated after the administration of both 5 and 10 mg/kg BW of KP102. The plasma GH responses to 5 and 10 mg/kg BW of KP102 were almost identical. The elevated GH levels after the first administration of KP102 tended to be maintained throughout the experiment, and a transient increase in plasma GH levels was observed after the second administration. However, the stimulatory effect of KP102 on GH release in the 3-mo-old goats was small and less abrupt than that in the 1-mo-old goats. The concentrations of insulin-like growth factor-I were not increased by KP102 during the brief sampling periods used in this experiment. These results show that the oral administration of the peptidergic GH secretogogue KP102 stimulates GH release in a ruminant species, and that the oral activity of KP102 on GH release is modified by the age.