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1.
A combined anterior pituitary (CAP) function test was assessed in eight healthy male beagle dogs. The CAP test consisted of sequential 30-second intravenous administrations of four hypothalamic releasing hormones in the following order and doses: 1 μg of corticotropin-releasing hormone (CRH)/kg, 1 μg of growth hormone-releasing hormone (GHRH)/kg, 10 μg of gonadotropinreleasing hormone (GnRH)/kg, and 10 μg of thyrotropin-releasing hormone (TRH)/kg. Plasma samples were assayed for adrenocorticotropin, cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. Each releasing hormone was also administered separately in the same dose to the same eight dogs in order to investigate any interactions between the releasing hormones in the combined function test.Compared with separate administration, the combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the responses to CRH, GHRH, and TRH. The combined administration of these four hypothalamic releasing hormones caused a 50% attenuation in LH response compared with the LH response to single GnRH administration. The side effects of the combined test were confined to restlessness and nausea in three dogs, which disappeared within minutes after the administration of the releasing hormones. It is concluded that with the rapid sequential administration of four hypothalamic releasing hormones (CRH, GHRH, GnRH, and TRH), the adenohypophyseal responses are similar to those occurring with the single administration of these secretagogues, with the exception of the LH response, which is lower in the CAP test than after single GnRH administration.  相似文献   

2.
The aim of the present study was to clarify the effects of hypothalamic dopamine (DA) on the secretion of growth hormone (GH) in goats. The GH‐releasing response to an intravenous (i.v.) injection of GH‐releasing hormone (GHRH, 0.25 μg/kg body weight (BW)) was examined after treatments to augment central DA using carbidopa (carbi, 1 mg/kg BW) and L‐dopa (1 mg/kg BW) in male and female goats under a 16‐h photoperiod (16 h light, 8 h dark) condition. GHRH significantly and rapidly stimulated the release of GH after its i.v. administration to goats (P < 0.05). The carbi and L‐dopa treatments completely suppressed GH‐releasing responses to GHRH in both male and female goats (P < 0.05). The prolactin (PRL)‐releasing response to an i.v. injection of thyrotropin‐releasing hormone (TRH, 1 μg/kg BW) was additionally examined in male goats in this study to confirm modifications to central DA concentrations. The treatments with carbi and L‐dopa significantly reduced TRH‐induced PRL release in goats (P < 0.05). These results demonstrated that hypothalamic DA was involved in the regulatory mechanisms of GH, as well as PRL secretion in goats.  相似文献   

3.
Tumor necrosis factor (TNF)‐α is a powerful macrophage cytokine released during infection, circulating in the blood to produce diverse effects in the organism. We examined the effect of recombinant bovine TNF‐α (rbTNF‐α) administration on hormone release in dairy cows during early lactation. Twelve non‐pregnant Holstein cows were treated subcutaneously with rbTNF‐α (2.5 µg/kg) or saline twice (at 11.00 and 23.00 hours). At 11.00 hours the next day, the cows were given growth hormone‐releasing hormone (GHRH, 0.25 µg/kg), thyrotrophin‐releasing hormone (TRH, 1.0 µg/kg), thyroid‐stimulating hormone (TSH, 10 µg/kg) or adrenocorticotropic hormone (500 µg/head) via the jugular vein. In the growth hormone‐releasing hormone challenge, the plasma growth hormone concentration was lower in the rbTNF‐α group than in the control (saline) group. The growth hormone and TSH responses to TRH were also smaller in the rbTNF‐α group than in the control. The plasma prolactin response to TRH was not affected by the rbTNF‐α treatment. In the TSH challenge, the rbTNF‐α‐treated cows had lower responses, as measured by plasma triiodothyronine and thyroxine, than the control cows. The rbTNF‐α treatment produced an increase in the basal plasma cortisol level, but the cortisol response to adrenocorticotropic hormone was the same level in both groups. The plasma concentrations of TNF‐α and interleukin‐1β in the cows were elevated by the rbTNF‐α treatment. The milk yield was reduced by the rbTNF‐α administration during 4 days. These data demonstrate that TNF‐α alters the secretion of pituitary and thyroid hormones in lactating cows. This effect may contribute to the suppression of the lactogenic function of the mammary gland observed in cases of coliform mastitis with high circulating TNF‐α levels.  相似文献   

4.
Effects of domperidone, a peripheral dopamine receptor antagonist, on secretion of LH and prolactin were studied during the luteal phase and following administration of PGF2 alpha. Since hyperprolactinemia has been reported to inhibit secretion of LH in ewes, effects of thyrotropin-releasing hormone (TRH) also were examined. Ewes 8-10 days post-estrus were assigned to be treated with: 1) vehicle (n = 5); 2) 0.3 mg domperidone (n = 6); 3) 1.0 mg domperidone (n = 6); 4) 3 micrograms TRH (n = 6); or 5) 10 micrograms TRH (n = 6) every 4 hours for 60 hr. Luteal regression was induced with PGF2 alpha at 12 hr after initiation of treatments. During the luteal phase, pulses of LH were more frequent (P less than .05) and the amplitudes of these were higher (P less than .05) in ewes treated with domperidone or TRH than in control ewes. These changes in LH occurred even though each treatment elevated markedly concentrations of prolactin in plasma. After induction of luteal regression, mean of LH and frequency of LH discharges were similar in all groups. However, in ewes treated with the 1.0 mg/4 hr dose of domperidone the pulse amplitude was greater than in the other groups (2.3 vs 1.1 ng/ml). Dose-response relationships and the magnitude of the prolactin release following domperidone or TRH varied with time. Treatments did not affect the timing of the LH surge or the increase in progesterone associated with the subsequent cycle.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

5.
Two experiments were conducted in ovariectomized, pituitary stalk-transected ewes to determine if dopamine (DA), norepinephrine (NE) or serotonin (5-HT) alter secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL). In experiment 1, ewes were infused (iv) with saline (control), DA (66 micrograms/kg/min), NE (6.6 micrograms/kg/min) or 5-HT (6.6 micrograms/kg/min). Treatments did not alter pulse frequency, but 5-HT increased (P less than .05) amplitude of pulses of LH and mean concentrations of LH, DA and NE were without effect on basal secretion of LH. DA but not NE or 5-HT decreased (P less than .05) the release of LH in response to gonadotropin hormone-releasing hormone (GnRH, 25 micrograms, im). Concentrations of FSH were not affected by treatments. Secretion of PRL was reduced (P less than .05) by treatment with DA and NE but not 5-HT. Each amine reduced (P less than .05) the release of PRL in response to thyrotropin-releasing hormone (TRH; 3 micrograms, im). In experiment 2, ewes were given DA at doses of 0, 0.66, 6.6 or 66.0 micrograms/kg/min, iv. No dose altered basal LH, but each dose reduced (P less than .05) basal and TRH-induced release of PRL. Key findings from these studies include direct pituitary action for: (1) 5-HT enhanced basal secretion of LH, (2) suppression of GnRH-induced secretion of LH by DA. (3) DA and NE inhibition of PRL secretion, and (4) DA, NE and 5-HT inhibition of release of PRL in response to TRH.  相似文献   

6.
Studies were conducted to determine the specificity and cause of altered pituitary hormone secretion when ewes ingest endophyte-infected (Acremonium coenophialum) GI-307 tall fescue (toxic fescue). Plasma concentrations of prolactin (PRL) but not growth hormone (GH) or thyroid stimulating hormone (TSH) in ewes grazing toxic fescue were significantly lower (P < .01) than concentrations measured in ewes grazing orchardgrass (OG). Comparing hormone secretory responses of ewes grazing each grasstype, ewes on toxic fescue released less PRL following thyrotropin releasing hormone (TRH) challenge than ewes on OG. TSH responses to TRH were not affected by grasstype. At this dose of TRH, GH secretion was not significantly affected in either group of ewes. In a separate study, dopamine hydrochloride (DA) was infused into control ewes to define the effect of a pure dopamine agonist on basal and TRH-stimulated secretion of PRL, GH and TSH. DA depressed both basal and TRH-stimulated secretion of PRL without affecting the basal concentrations or responses of GH or TSH. Based on the assumption that the active agent in toxic fescue responsible for the observed hypoprolactinemia was a dopaminergic agonist, haloperidol (HAL), a DA receptor blocking drug, was administered to ewes grazing toxic fescue or OG. HAL evoked significant PRL secretion unaccompanied by any GH or TSH effect in both toxic fescue and OG ewes. Administration of HAL resulted in a gradual increase over 4 hr in PRL in toxic fescue ewes and prolonged the duration of the PRL response to TRH. No differences in circulating plasma concentrations of DA, epinephrine or norepinephrine were measured in ewes on troxic fescue or OG.

Alterations in pituitary hormone secretion due to toxic factors in fescue were confined to PRL. Hormone secretory responses to TRH and HAL suggest that the effects on PRL are mediated through dopamine-like activity in toxic fescue.  相似文献   


7.
Light horse mares, stallions, and geldings were used to 1) extend our observations on the thyrotropin releasing hormone (TRH) inhibition of GH secretion in response to physiologic stimuli and 2) test the hypothesis that stimulation of endogenous TRH would decrease the normal rate of GH secretion. In Exp. 1 and 2, pretreatment of mares with TRH (10 microg/kg BW) decreased (P < 0.001) the GH response to exercise and aspartate infusion. Time analysis in Exp. 3 indicated that the TRH inhibition lasted at least 60 min but was absent by 120 min. Administration of a single injection of TRH to stallions in Exp. 4 increased (P < 0.001) prolactin concentrations as expected but had no effect (P > 0.10) on GH concentrations. Similarly, 11 hourly injections of TRH administered to geldings in Exp. 5 did not alter (P > 0.10) GH concentrations either during the injections or for the next 14 h. In Exp. 5, it was noted that the prolactin and thyroid-stimulating hormone responses to TRH were great (P < 0.001) for the first injection, but subsequent injections had little to no stimulatory effect. Thus, Exp. 6 was designed to determine whether the inhibitory effect of TRH also waned after multiple injections. Geldings pretreated with five hourly injections of TRH had an exercise-induced GH response identical to that of control geldings, indicating that the inhibitory effect was absent after five TRH injections. Retrospective analysis of pooled, selected data from Exp. 4, 5, and 6 indicated that endogenous GH concentrations were in fact lower (P < 0.01) from 45 to 75 min after TRH injection but not thereafter. In Exp. 7, 6-n-propyl-2-thiouracil was fed to stallions to reduce thyroid activity and hence thyroid hormone feedback, potentially increasing endogenous TRH secretion. Treated stallions had decreased (P < 0.01) concentrations of thyroxine and elevated (P < 0.01) concentrations of thyroid-stimulating hormone by d 52 of feeding, but plasma concentrations of GH and prolactin were unaffected (P > 0.10). In contrast, the GH response to aspartate and the prolactin response to sulpiride were greater (P < 0.05) in treated stallions than in controls. In summary, TRH inhibited exercise- and aspartate-induced GH secretion. The duration of the inhibition was at least 1 h but less than 2 h, and it waned with multiple injections. There is likely a TRH inhibition of endogenous GH episodes as well. Reduced thyroid feedback on the hypothalamic-pituitary axis did not alter basal GH and prolactin secretion.  相似文献   

8.
To determine whether long-term administration of growth hormone (GH)-releasing factor (GRF) and(or) thyrotropin-releasing hormone (TRH) alters ovarian follicular fluid (FFL) concentrations of insulin-like growth factor-I (IGF-I), progesterone, and estradiol (E2), and follicular growth, Friesian x Hereford heifers (n = 47; 346 +/- 3 kg) were divided into the following four groups: control (vehicle; n = 11); 1 micrograms GRF (human [Des NH2 Tyr1, D-Ala2, Ala15] GRF [1-29]-NH2).kg-1 BW.d-1 (n = 12); 1 microgram TRH.kg-1 BW.d-1 (n = 12); or GRF + TRH (n = 12). Daily injections (s.c.) continued for 86 d. On d 89, heifers that had been synchronized were slaughtered and ovaries were removed. Follicles were grouped by magnitude of diameter into the three following sizes: 1 to 3.9 mm (small, n = 55), 4.0 to 7.9 mm (medium, n = 63), and greater than or equal to 8 mm (large, n = 71). Growth hormone-releasing factor and(or) TRH did not affect (P greater than .10) IGF-I concentrations in FFL of any follicle size group. Growth hormone-releasing factor increased (P less than .06) size (means +/- pooled SE) of large follicles (14.7 vs 13.0 +/- .6 mm). Growth hormone-releasing factor also increased (P less than .05) progesterone concentrations 4.4-fold above controls in FFL of medium-sized follicles but had no effect on progesterone in FFL of the small or large follicles. Thyrotropin-releasing hormone did not alter FFL progesterone or E2 concentrations in any follicle size group. We conclude that the GRF and(or) TRH treatments we employed did not affect intra-ovarian IGF-I concentrations, but GRF may alter steroidogenesis of medium-sized follicles and growth of large follicles.  相似文献   

9.
Fasting has severe effects on thyroid metabolism in the chicken: plasma thyroxine (T4) concentrations increase, whereas 3′,5,3-triiodothyronine (T3) concentrations decrease. In the present report we studied the effect of fasting at the level of: 1) the pituitary (plasma thyrotropin (TSH) concentrations; the sensitivity of thyrotrophs to corticotropin-releasing hormone (CRH) and TSH-releasing hormone (TRH)); and 2) the hypothalamus (TRH content). A regulatory role of corticosterone is discussed. One day of fasting resulted in a drop in plasma TSH concentrations. Fed and nonfed animals were treated with ovine CRH (oCRH) or TRH. The sensitivity of thyrotrophs to the respective hypothalamic hormones was increased when animals were subjected to a 1-d period of fasting. A 75% (TRH) and 50% (oCRH) increase in plasma TSH was recorded in fasted animals, whereas both secretagogues did not evoke any response in their fed counterparts. The drop in plasma TSH cannot, therefore, be attributed to a loss in sensitivity of thyrotrophs to hypothalamic stimulatory control. In an identical experiment, plasma TSH concentrations decreased, whereas hypothalamic TRH content was higher in fasted animals, suggesting a decreased hypothalamic TRH release toward the pituitary. In both fasting experiments, plasma corticosterone concentrations were increased after 1 d of fasting. Because an iv injection of corticosterone-elevated hypothalamic TRH contents and decreased plasma TSH concentrations, a corticosterone-induced TSH decrease during fasting is suggested through an action at the level of the hypothalamus.  相似文献   

10.
Several different amino acids and peptides control secretion of adenohypophysial hormones and this control may be indirect, via the modulation of hypothalamic hormone secretion. Indeed, classical hypothalamic hormones (e.g., gonadotropin-releasing hormone [GnRH], growth hormone-releasing hormone [GHRH], somatostatin, etc.) may be released into the hypothalamo-hypophysial portal vasculature, travel to the adenohypophysis and there stimulate or inhibit secretion of hormones. Alternatively, some amino acids and peptides exert direct stimulatory or inhibitory effects on the adenohypophysis, thereby impacting hormone secretion. In swine, the most extensively studied modulators of adenohypophysial hormone secretion are the excitatory amino acids (ExAA), namely glutamate and aspartate, and the endogenous opioid peptides (EOP). In general, excitatory amino acids stimulate release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin (PRL). Secretion of adenohypophysial hormones induced by ExAA is primarily, but perhaps not exclusively, a consequence of action at the central nervous system. By acting primarily at the level of the central nervous system, EOP inhibit LH secretion, stimulate GH release and depending on the animal model studied, exert either stimulatory or inhibitory influences on PRL secretion. However, the EOP also inhibited LH release by direct action on the adenohypophysis. More recently, peptides such as neuropeptide-Y (NPY), orexin-B, ghrelin, galanin, and substance P have been evaluated for possible roles in controlling adenohypophysial hormone secretion in swine. For example, NPY, orexin-B, and ghrelin increased basal GH secretion and modulated the GH response to GHRH, at least in part, by direct action on the adenohypophysis. Secretion of LH was stimulated by orexin-B, galanin, and substance P from porcine pituitary cells in vitro. Because the ExAA and various peptides modulate secretion of adenohypophysial hormones, these compounds may play an important role in regulating swine growth and reproduction.  相似文献   

11.
The aim of the present study was to clarify the relationship between hypothalamic dopamine (DA) and salsolinol (SAL) for the secretion of prolactin (PRL) in goats. SAL or thyrotropin‐releasing hormone (TRH) was intravenously injected into female goats treated with or without the D2 DA receptor antagonist haloperidol (Hal), which crosses the blood‐brain barrier, and the PRL‐releasing response to SAL was compared with that to TRH. PRL‐releasing responses to SAL, Hal, and Hal plus SAL were also examined after a pretreatment to augment central DA using carbidopa (Carbi) and L‐dopa. The PRL‐releasing response to Hal alone was greater than that to SAL or TRH alone. The PRL‐releasing response to Hal plus SAL was similar to that of Hal alone. In contrast, the PRL‐releasing response to Hal plus TRH was greater than that to TRH or Hal alone. The treatment with Carbi plus L‐dopa inhibited SAL‐ and Hal‐induced PRL secretion. The inhibition of the PRL‐releasing response to SAL disappeared when SAL was injected with Hal. These results indicate that the mechanisms underlying the SAL‐induced PRL response differ from those of TRH, and suggest that hypothalamic DA and its synthesis is associated in part with SAL‐induced PRL secretion in goats.  相似文献   

12.
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.  相似文献   

13.
Serum concentrations of thyrotropin (TSH), prolactin, thyroxine, and 3,5,3'-triiodothyronine in 15 euthyroid dogs and 5 thyroidectomized and propylthiouracil-treated dogs after thyrotropin-releasing hormone (TRH) administration were measured. Although thyroidectomized and propylthiouracil-treated dogs had higher (P less than 0.01) base-line concentrations of TSH in serum than did euthyroid dogs, concentrations of TSH after TRH administration varied at 7.5, 15, and 30 minutes with 14 of 45 samples obtained from healthy dogs having lower TSH concentrations than before TRH challenge. Similarly, concentrations of 3,5,3'-triiodothyronine in the serum of euthyroid dogs 4 hours after TRH administration were similar (P less than 0.05) to concentrations before TRH challenge. Although the mean concentration of thyroxine in serum was elevated (P less than 0.05) 4 hours after administration of TRH to euthyroid animals, as compared with base-line levels, the individual response was variable with concentrations not changing or decreasing in 4 dogs. Therefore, the TRH challenge test as performed in the current investigation was of limited value in evaluating canine pituitary gland function. Although mean concentrations of TSH in serum were higher (P less than 0.05) in euthyroid dogs after TRH administration, the response was too variable among individual animals for accurate evaluation of pituitary gland function. Concentrations of prolactin in the sera of dogs after TRH administration, confirmed previous reports that exogenously administered TRH results in prolactin release from the canine pituitary and indicated that the TRH used was biologically potent.  相似文献   

14.
The pituitary gland, occupying a central position in the hypothalamo-pituitary thyroidal axis, produces thyrotropin (TSH), which is known to stimulate the thyroid gland to synthetize and release its products, thyroid hormones. TSH is produced by a specific cell population in the pituitary, the so-called thyrotropes. Their secretory activity is controlled by the hypothalamus, releasing both stimulatory and inhibitory factors that reach the pituitary through a portal system of blood vessels. Based on early experiments in mammals, thyrotropin-releasing hormone (TRH) is generally mentioned as the main stimulator of the thyrotropes. During the past few decades, it has become clear that the hypophysiotropic function of the hypothalamus is more complex, with different hormonal axes interacting with each other. In the chicken, it was found that not only TRH, but also corticotropin-releasing hormone (CRH), the main stimulator of corticotropin release, is a potent stimulator of TSH secretion. Somatostatin (SRIH), a hypothalamic factor known for its inhibitory effect on growth hormone secretion, was demonstrated to blunt the TSH response to TRH and CRH. In this review we summarize the latest studies concerning the "interaxial" hypothalamic control of TSH release in the chicken, with a special emphasis on the molecular components of these control mechanisms. It remains to be demonstrated if these findings could also be extrapolated to other species or classes of vertebrates.  相似文献   

15.
Primary hypothyroidism in dogs is associated with increased release of growth hormone (GH). In search for an explanation we investigated the effect of intravenous administration of thyrotropin-releasing hormone (TRH, 10 microg/kg body weight) on GH release in 10 dogs with primary hypothyroidism and 6 healthy control dogs. The hypothyroid dogs had a medical history and physical changes compatible with hypothyroidism and were included in the study on the basis of the following criteria: plasma thyroxine concentration < 2 nmol/l and plasma thyrotropin (TSH) concentration > 1 microg/l. In addition, (99m)TcO(4)(-) uptake during thyroid scintigraphy was low or absent. TRH administration caused plasma TSH concentrations to rise significantly in the control dogs, but not in the hypothyroid dogs. In the dogs with primary hypothyroidism, the mean basal plasma GH concentration was relatively high (2.3+/-0.5 microg/l) and increased significantly (P=0.001) 10 and 20 min after injection of TRH (to 11.9+/-3.5 and 9.8+/-2.7 microg/l, respectively). In the control dogs, the mean basal plasma GH concentration was 1.3+/-0.1 microg/l and did not increase significantly after TRH administration. We conclude that, in contrast to healthy control dogs, primary hypothyroid dogs respond to TRH administration with a significant increase in the plasma GH concentration, possibly as a result of transdifferentiation of somatotropic pituitary cells to thyrosomatotropes.  相似文献   

16.
The aim of the present study was to clarify the effect of melatonin (MEL) on the salsolinol (SAL)‐induced release of prolactin (PRL) in goats. Female goats were kept at 20°C with 16 h of light, 8 h of darkness, and orally administered saline or MEL for 5 weeks. A single intravenous (i.v.) injection of saline (controls), SAL, thyrotropin‐releasing hormone (TRH) or a dopamine receptor antagonist, sulpiride, was given to the goats 3 weeks after the first oral administrations of saline or MEL, and the responses were compared. The mean basal plasma PRL concentrations in the control group were higher for the saline treatments than MEL treatments (P < 0.05). SAL as well as TRH and sulpiride stimulated the release of PRL promptly after each injection in both the saline‐ and MEL‐treated groups (P < 0.05). The area under the response curve of PRL for the 60‐min period after the i.v. injection of SAL, TRH and sulpiride in the saline‐treated group was greater than each corresponding value in the MEL‐treated group (P < 0.05). These results show that daily exposure to MEL under a long day length reduces the PRL‐releasing response to SAL as well as TRH and sulpiride in goats.  相似文献   

17.
本试验旨在研究植物甾醇对雌性小鼠生长及生殖激素的影响。选用50只35日龄雌性小鼠,适应1周后随机分为5组,分别为：对照组、植物油组（给予0.1 mL植物油）及植物甾醇低、中、高三个剂量组（每日灌胃20、80和320 mg/kg植物甾醇）。连续灌胃3周,第1天和第22天称取小鼠体重,然后眼球采血,制备血清,对小鼠血清中的雌二醇、孕酮、催乳素水平进行检测,研究不同添加量的植物甾醇对小鼠生长及生殖激素的影响。结果显示：与对照组相比,植物油组小鼠体增重差异显著（P＜0.05）。与植物油组相比,植物甾醇处理组小鼠体增重先升高后降低,但差异不显著（P＞0.05）。植物甾醇对小鼠血清E2水平有不同程度的提高,其中中剂量组小鼠的雌二醇水平最高（270.52＆#177;18.10 pmol/L）;随着植物甾醇灌胃剂量的增加,小鼠孕酮水平都有不同程度的下降,其中植物甾醇中剂量组小鼠血清孕酮水平显著低于对照组（P＜0.05）。植物甾醇灌胃组小鼠催乳素水平与对照组相比,差异不显著（P＞0.05）。表明低剂量植物甾醇可提高KM雌性小鼠的体增重;植物甾醇能提高KM雌性小鼠血清雌二醇水平,但对孕酮和催乳素的作用不显著。  相似文献   

18.
A radioimmunoassay (RIA) based on anti-equine prolactin antiserum and radioiodinated canine prolactin was used to assess the dose response of plasma prolactin to thyrotropin releasing hormone (TRH) in mares in the nonbreeding season (winter) and in mares in estrus in the breeding season (summer). Mares were administered TRH intravenously and blood samples were collected via jugular catheters at −15, 0, 15, 30, 45, 60, 90, 120, 180 and 240 min relative to injection. Doses of TRH were 0, .08, .40, 2.0 and 10.0 mg per mare (n = 3 per dose within each season). The prolactin response was assessed by absolute hormonal concentrations before and after TRH injection and by net area under the curve. Prolactin concentrations in plasma before injection of TRH were higher (P < .01) in estrous mares in summer than in anestrous mares in winter (4.8 vs 1.3 ng/ml). Moreover, there was a greater (P < .01) response to TRH injection in estrous mares than in anestrous mares. Based on areas under the curve, there was an effect of season (P < .01) and of TRH dose (P < .01) as well as a season-dose interaction (P < .01). In general, there was little or no prolactin response to any dose of TRH in anestrous mares in winter when pre-TRH concentrations were low. In contrast, there was an increase in the prolactin response with increasing doses of TRH up to 2.0 mg in estrous mares in summer; 2.0 and 10.0 mg of TRH resulted in similar prolactin secretion. We conclude 1) that prolactin secretion in the horse is stimulated by TRH as has been reported for other species and 2) that prolactin concentrations and the TRH-induced secretion of prolactin are greater in estrous mares in summer than in anestrous mares in winter.  相似文献   

19.
The interaction of human pancreatic growth hormone releasing factor (hpGRF) and thyrotropin releasing hormone (TRH) on chicken growth hormone (cGH) release in vivo and possible noradrenergic involvement on TRH-induced stimulation of cGH in vivo were examined. Four-week old cockerels (1 kg) were injected intravenously with hpGRF (1.0 μg/bird), TRH (0.1 μg/bird), or hpGRF (1.0 μg/bird) in combination with TRH (0.1 μg/bird). Five min after the injection, blood samples were collected and serum concentrations of cGH were determined by a homologous RIA. The results showed that hpGRF and TRH were potent stimulators of cGH release, 5- and 6-fold over the control birds, respectively, and that hpGRF and TRH administered in combination produced a synergistic stimulation of cGH release (>20 fold). In separate experiments, pretreatment with alpha-methyl-para-tyrosine (250 mg/bird) for 2 hours resulted in complete suppression of the TRH stimulatory effect on cGH release but not the stimulatory effect of hpGRF. Pretreated with phenoxybenzamine hydrochloride (20 mg/bird) or diethyl-dithiocarbamate (500 mg/bird) also resulted in complete suppression of TRH-induced cGH release. These results indicate that hpGRF acts directly at the pituitary and TRH acts at the hypothalamus in addition to the pituitary in stimulating cGH release, possibly mediated through the noradrenergic neurons. HpGRF and TRH were potent releasers of cGH and their stimulation was potentiated when administered together.  相似文献   

20.
The effects of intravenous (IV) and intracerebroventricular (ICV) administration of either bovine growth hormone releasing hormone (GRF) or thyrotrophin releasing hormone (TRH) on plasma growth hormone (GH) and glucose levels have been examined in sheep. Intravenous GRF 1-29NH2 at 3 and 30 micrograms stimulated an increase in GH levels in a dose-dependent fashion; administration of GRF into a lateral cerebral ventricle, however, produced a smaller GH response which was similar at these two doses. Evaluation of somatostatin levels in petrosal sinus blood (which collects pituitary effluent blood) showed that ICV administration of GRF stimulated a release of somatostatin into the blood. Furthermore, concurrent administration of GRF and a potent anti-somatostatin serum ICV resulted in a much enhanced release of GH which was similar to that obtained with a comparable dose of GRF given IV. TRH (as another putative GH-secretagogue) was also administered both IV and ICV. When given IV, 200 micrograms (but not 100 micrograms) TRH produced an elevation in GH levels. By contrast, when 5 micrograms TRH was given ICV there was a decrease in circulating GH levels, but no change in plasma somatostatin concentrations. These results indicate that the smaller GH response to ICV- compared with IV-administered GRF is due to the release of somatostatin within the brain. In addition, it would seem that TRH is not a physiological GH-secretagogue in sheep.  相似文献   

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