Growth Hormone and ACTH Secretion: Evidence for an Inverse Relationship in Rats

Kokka, Norio; Jf, Garcia; George, Rani Mary; Hw, Elliot

doi:10.1210/endo-90-3-735

Cited by 107 publications

(29 citation statements)

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“…It can also be seen that treatment with either [D-Ala2,D-Leu5]enkephalin or fl-endorphin significantly reduced the decline in dopamine concentration at the same time point (15 min after injection of the opioid). Similar doses of opioids have been shown to increase blood prolactin levels in rats (2,3,5). As is the case for morphine, the actions of the endorphins were blocked by naloxone pretreatment, but in this case the blockade was not total at the naloxone dose used.…”

mentioning

confidence: 76%

“…It is well known from previous investigations on the pharmacology of narcotics that narcotic drugs affect the secretion of several pituitary hormones, including prolactin, growth hormone, vasopressin, and adrenocorticotropic hormone (ACTH). Morphine is a potent releaser of prolactin, growth hormone, and vasopressin (1)(2)(3)(4). Recently, it has been shown that enkephalin analogs can also increase blood prolactin levels (5).…”

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confidence: 99%

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Morphine and endorphins modulate dopamine turnover in rat median eminence.

Deyo¹,

Swift²,

Miller³

1979

Proc. Natl. Acad. Sci. U.S.A.

134

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There is evidence that some of the actions of both endogenous and exogenous opioids (e.g., stimulation of prolactin release) are mediated by interaction with catecholaminergic systems. Morphine (1.67, 5, and 15 mg/kg of body weight, intraperitoneally) altered dopamine turnover as measured by the a-methyl-p-tyrosine method in the median eminence, neostriatum, and frontal cortex of male Sprague-Dawley rats. The turnover rate of dopamine was reduced in the median eminence and frontal cortexbut accelerated in the neostriatum. In the frontal cortex all doses were effective in decreasing dopamine turnover; however, in the median eminence the lowest dose of morphine did not significantly alter dopamine turnover. All three doses accelerated dopamine turnover in the neostriatum. Naloxone effectively reversed the effects of morphine at all doses in all brain areas, whereas it had no effect on turnover when given alone. In the median eminence, neostriatum, and frontal cortex, intraventricular injection of D-Ala2,D-Leu5J enkephalin (25 Mug) or fl-endorphin (15 ,g) produced the same effects on dopamine turnover as morphine. The actions of these peptides were blocked by naloxone. It is hypothesized that opiates and opioid peptides increase prolactin release by reducing the activity of the tuberoinfundibular dopaminergic system.Since the discovery of the endorphins and the enkephalins, peptides with opiate agonist activity, intensive investigations have been carried out in order to define the functions of these peptides in the nervous system. It is becoming evident that one such important role may be in the control of the release of hormones from the pituitary gland. It is well known from previous investigations on the pharmacology of narcotics that narcotic drugs affect the secretion of several pituitary hormones, including prolactin, growth hormone, vasopressin, and adrenocorticotropic hormone (ACTH). Morphine is a potent releaser of prolactin, growth hormone, and vasopressin (1-4). Recently, it has been shown that enkephalin analogs can also increase blood prolactin levels (5).Immunohistochemical studies on enkephalin distribution within the brain have defined several potential enkephalinergic pathways that may serve to regulate the release of these hormones (6). Thus, an enkephalin-containing neuronal system projecting from the paraventricular nucleus of the hypothalamus to the pars nervosa of the pituitary may serve to regulate the release of vasopressin (7). In addition, it has been shown that the median eminence contains a large number of enkephalinergic nerve endings (6). Because it is known that endorphins and morphine do not produce their releasing actions on pituitary prolactin by direct action on pituitary lactotrophs (8, 9), it therefore appears that this action of these opioid compounds is mediated at the level of the hypothalamus.Because the main hypothalamic control of prolactin secretion is mediated by hypothalamic dopaminergic neurons (10), we investigated the possibility that the releasing effects of...

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mentioning

confidence: 76%

mentioning

confidence: 99%

Morphine and endorphins modulate dopamine turnover in rat median eminence.

Deyo¹,

Swift²,

Miller³

1979

Proc. Natl. Acad. Sci. U.S.A.

134

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“…It is most likely tenable that the large granules may be made up by increasing the dimension of the small ones. Many investigators (Pecile et al, 1965;Schalch, 1967;Meyer and Knobil, 1967;Caracia et al, 1968;Schalch and Reichlin, 1968 ;Brown et al, 1971;Kokka et al, 1972. ) paid attention to a close relationship between the secretions of ACTH and GH.…”

Section: Discussionmentioning

confidence: 99%

Fine Structure of Pituitary Acidophils in Thyroidectomized Rats with or without the Treatment with Thyroxine and Dexamethasone

Harumiya

1972

Endocrinol Japon

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SynopsisElectron microscopic study was made on rat anterior pituitaries in an attempt to clarify the causal mechanism of "loss of acidophils" which could be detected with the light microscope following thyroidectomy. In the advancing days after thyroidectomy, the acidophils (somatotrophs) were gradually deprived of their large granules whose diameter was about 350 mu. There was evidence in vivo for the first time that there were some acidophils containing only the small granules, about 130 mu in diameter, after the 7th postoperative day. This clearly showed the simultaneous existence of two different sizes of granules in the same acidophils. As time elapsed, the large granules dispersed from the acidophils. After the 30th day these acidophils began to adjust their shape into the polygonal cells. Eventually, the acidophils completely lacking granules of either size occassionally appeared on the 90th and 200th days. Thus thyroidectomy had a strong influence to release the large granules, whereas an influence to release the small ones was not remarkable. The replacement injection of thyroxine into the thyroidectomized rats efficaciously reproduced the large granules which were generally considered to be responsible for GH storage. The repeated administrations of dexamethasone to the thyroidectomized rats resulted in the increase in number of small granules that were thought by us to be the storage carriers of ACTH. On the other hand, this compound alleviated loss of large granules following thyroidectomy. The final fate of acidophils after thyro:c.ectomy was, however, still vague because of the equivocal distinguishment of these degranulated acidophils from the immature basophils. Thus, the "loss of acidophils" may not mean the intrinsic disappearance of the cells themselves, but represent a transient loss of the large dense granules in the remaining acidophils.

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“…Further, this loss of blood was presumed not to be stressful for the rat, since GH secretion has been shown to be suppressed by stress (Kokka, Garcia, George & Elliott, 1972;Terry, Saunders, Audet, Willoughby, Brazeau & Martin, 1977), whereas secretion continued through the 6-h sampling period in immature rats (Kawakami et al 1983). …”

Section: Blood Samplingmentioning

confidence: 99%

Relationship between the three‐hour‐period sleep‐wakefulness cycle and growth hormone secretion in the immature rat.

Kawakami¹,

Kimura²,

Tsai³

1984

The Journal of Physiology

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SUMMARY1. The temporal pattern of growth hormone (GH) secretion throughout a day and its correlation with the sleep-wakefulness cycle in the 29-31-day-old female rat were studied by serial blood sampling through an intracardiac cannula at 10-min intervals. Electroencephalograms (e.e.g.s) recorded continuously during blood sampling periods were scored into wakefulness and sleep, and the amount of sleep for every 10 min was plotted against the GH value as assessed by radio-immunoassay.2. By analysis of the power spectrum using the least-squares method, the time series of GH concentration was found to have a periodicity of approximately 3 0 h in any of the 6-h periods sampled, beginning at 12.00, 18.00, 00.00 and 06.00 h, and in either sex.3. The peak time which was estimated for the time series of GH concentrations was found to occur consistently around 02.00-03.00, 05.00-06.00, 08.00-09.00, 11.00-12.00, 14.00-15.00, 17.00-18.00, 20.00-21.00 and 23.00-24.00 h in either the male or the female rat.4. The cross-correlation analysis performed between the time series of the amount of sleep and the GH concentration, which were obtained for the 6-h period from 12.00 to 18.00 h, revealed a significant positive correlation between the GH level and the amount of sleep during the preceding 10 min.5. The time series of the amount of sleep over a 24-h period from the data obtained in the continuous recording of e.e.g.s from 27 to 31 days of age revealed an ultradian rhythm with a periodicity of approximately 3 0 h.6. These findings indicate that the rat GH secretary rhythm with a 3-0-h periodicity develops by 30 days of age in both sexes, relating to the 3-0-h-period ultradian rhythm of the sleep-wakefulness cycle entrained by the light cycle.

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Growth Hormone and ACTH Secretion: Evidence for an Inverse Relationship in Rats

Cited by 107 publications

References 0 publications

Morphine and endorphins modulate dopamine turnover in rat median eminence.

Morphine and endorphins modulate dopamine turnover in rat median eminence.

Fine Structure of Pituitary Acidophils in Thyroidectomized Rats with or without the Treatment with Thyroxine and Dexamethasone

Relationship between the three‐hour‐period sleep‐wakefulness cycle and growth hormone secretion in the immature rat.

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