Stimulation of release of growth hormone from the anterior pituitary by α-melanocyte-stimulating hormone: a possible mechanism for induction of pseudopregnancy in the rat

1988 ◽  
Vol 118 (3) ◽  
pp. 465-470
Author(s):  
M. Volosin ◽  
M. E. Celis

ABSTRACT In hypophysectomized rats on day 1 of dioestrus, as well as on day 4 of pseudopregnancy, α-MSH (continuous infusion of 1 μg/h) failed to maintain serum concentrations of progesterone. On the other hand, α-MSH did not modify the increase induced by ACTH (1 μg/μl as an infusion plus two additional daily injections of 30 μg/μl), prolactin (200 μg/0·2 ml at 12-h intervals) or GH (300 μg/0·2 ml twice daily) on serum concentrations of progesterone in such rats. However, in intact rats α-MSH caused a significant rise in serum concentrations of GH on day 1 and day 2 of dioestrus. Continuous infusion of α-MSH produced an increase in serum concentrations of GH at 12.00 and 14.00 h on day 1 of dioestrus and at 07.00 h on day 2. It is therefore suggested that α-MSH may exert its effect by facilitating the secretion of GH, which in turn may induce the release of progesterone. J. Endocr. (1988) 118, 465–470

1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.


1972 ◽  
Vol 71 (1) ◽  
pp. 179-190 ◽  
Author(s):  
Lars-Eric Tisell ◽  
Lennart Angervall

ABSTRACT The growth of the ventral and dorsolateral prostate, the coagulating glands and the seminal vesicles was studied in force-fed hypophysectomized castrated adrenalectomized rats following daily injections for fourteen days of protamine zinc insulin or cortisone acetate alone or in combination. Cortisone was given in daily doses of 3 mg and insulin was administered in increasing daily doses of protamine zinc insulin up to 8 IU. Cortisone alone induced slight histological stimulation of the epithelium of the coagulating glands, while no stimulation was demonstrated in the other accessory reproductive organs. After insulin alone the weight of the accessory reproductive organs was slightly increased but no stimulation was demonstrated histologically. Cortisone and insulin given in combination induced distinct signs of stimulation of all the accessory reproductive organs as assesed by histological examination and weight determination of the organs. The results indicate that in the rat the growth stimulating effect of cortisone on the male accessory reproductive organs is markedly decreased or abolished in the absence of the anterior pituitary. Insulin can act synergistically with cortisone in promoting the growth of the accessory reproductive organs through effects which are not dependent on the presence of the adrenal glands or the anterior pituitary.


1974 ◽  
Vol 142 (2) ◽  
pp. 295-300 ◽  
Author(s):  
J. George Schofield ◽  
Margaret McPherson

The release of growth hormone from heifer anterior pituitary slices and the cyclic AMP content of the slices were increased by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, both increases being related to inhibitor concentration over the range 0.1–1.0mm. Neither Ba2+(6.9 or 2.3mm), K+(72mm), nor p-chloromercuribenzoate (20μm) had any effect on pituitary cyclic AMP content over a 20min period. 3-Isobutyl-1-methylxanthine potentiated the release of growth hormone in response to Ba2+(2.3mm) and K+(24mm), but the degree of potentiation did not depend on inhibitor concentration in the same way as did tissue cyclic AMP content. 3-Isobutyl-1-methylxanthine decreased the concentration of K+required to give maximum stimulation of growth-hormone release, but did not significantly increase the maximum response to Ba2+. Growth-hormone release in the presence of prostaglandin E2 (1μm) was increased by 3-isobutyl-1-methylxanthine and was inhibited by the prostaglandin antagonist, 7-oxa-13-prostynoic acid, although this antagonist increased the pituitary cyclic AMP concentration and potentiated the prostaglandin E2-induced rise in cyclic AMP content. The stimulation of growth-hormone release by p-chloromercuribenzoate was not potentiated by 3-isobutyl-1-methylxanthine. The data suggest that Ba+and K+act at the same point in the secretory process as 3-isobutyl-1-methylxanthine, although by a different mechanism, and that p-chloromercuribenzoate has a different point of action.


1977 ◽  
Vol 154 (4) ◽  
pp. 573-577 ◽  
Author(s):  
A. E. Panerai ◽  
G. L. Rossi ◽  
D. Cocchi ◽  
I. Gil-Ad ◽  
V. Locatelli ◽  
...  

1965 ◽  
Vol 208 (5) ◽  
pp. 1026-1030 ◽  
Author(s):  
Robert Cade ◽  
Theresa Perenich

The effect of sodium deprivation on adrenal blood flow and secretion of aldosterone and corticosterone was measured in intact rats. The changes induced by sodium deprivation were then compared with those resulting from infusion of angiotensin and vasopressin into hypophysectomized-nephrectomized animals and with the effect of angiotensin in oil given chronically to hypophysectomized rats. Sodium deprivation caused increased secretion of aldosterone but decreased secretion of corticosterone. Small doses of angiotensin infused acutely increased secretion of corticosterone but had no effect on aldosterone secretion. Large doses of either polypeptide increased both corticosterone and aldosterone. Chronic administration of small doses of angiotensin in oil increased corticosterone secretion but had no effect on secretion of aldosterone. Because angiotensin and vasopressin increase while sodium deprivation decreases secretion of corticosterone, it is concluded that neither of these polypeptides is responsible for the stimulation of aldosterone secretion which occurs with sodium deprivation.


1968 ◽  
Vol 42 (3) ◽  
pp. 465-475 ◽  
Author(s):  
T. C. LEE ◽  
B. van der WAL ◽  
D. de WIED

SUMMARY Studies of the rate of aldosterone production in vitro of adrenals of rats hypophysectomized before dietary sodium restriction showed that hypophysectomy not only prevented the increases in aldosterone production observed in intact, Na-deprived rats, but also depressed the level of aldosterone production to below that of intact rats maintained on a normal diet. Rats hypophysectomized for a similar period of time but maintained on the normal diet showed a similar decrease. Experiments on adeno- and neuro-hypophysectomized rats indicated that the pituitary factor required for the normal mineralocorticoid response to dietary sodium restriction resides in the anterior pituitary. Treatment of hypophysectomized rats during dietary sodium restriction with doses of a long-acting corticotrophin (ACTH) prevented adrenal atrophy and maintained a normal glucocorticoid response to intravenous injections of ACTH, but failed to increase aldosterone production rates in vitro to levels above that of intact rats on a normal diet; it also failed to restore the enhanced adrenocortical sensitivity to the stimulating effect of aldosterone production of intravenously injected ACTH which is characteristic of acutely hypophysectomized, Na-deficient rats. Treatment with anterior pituitary powder (8–12 mg./day) for similar periods, however, restored the aldosterone production of adrenals in vitro of hypophysectomized, Na-deprived rats to levels nearly indistinguishable from those of acutely hypophysectomized, Na-deprived controls. The same doses of anterior pituitary powder were shown not to have any demonstrable effect on the aldosterone production of adrenals in vitro of intact rats on a normal diet. These results are interpreted as indicating the existence of a pituitary factor other than ACTH which stimulates aldosterone secretion. This factor does not appear to act directly on the adrenal cortex or to stimulate the secretion of specific glomerulotropic substances, but probably exerts its effect by maintaining the normal functional capacity of some as yet undefined tissues which secrete glomerulotropic substances in response to dietary sodium restriction.


1993 ◽  
Vol 294 (1) ◽  
pp. 159-165 ◽  
Author(s):  
P K Srivastava ◽  
D J Waxman

The sex-dependent expression and growth hormone (GH) regulation of rat liver glutathione S-transferase (GST) was examined using oligonucleotide probes that distinguish between closely related class Alpha (Ya1, Ya2, Yc) and class Mu (Yb1, Yb2, Yb3) GST mRNAs [Waxman, Sundseth, Srivastava and Lapenson (1992) Cancer Res. 52, 5797-5802]. Northern-blot analysis revealed that the steady-state levels of GST Ya1, Yb1 and Yb2 mRNAs are 2.5-3-fold higher in male as compared with female rat liver. In contrast, GST Yc and Ya2 mRNAs were expressed at a 2-3-fold higher level in female rat liver. Microsomal GST mRNA did not exhibit significant sex-dependent differences in rat liver. Treatment of male rats with GH by continuous infusion suppressed expression of the male-dominant GST Ya1, Yb1 and Yb2 mRNAs to levels at or below those found in female rat liver. This suppressive effect of GH was liver-specific, insofar as GH treatment did not alter kidney GST Ya1 mRNA levels. Hypophysectomy increased expression of the male-dominant GSTs, particularly in female rats (e.g. 8-fold elevation of GST Ya1 mRNA). GST Yc mRNA was increased approx. 2-fold in hypophysectomized males, indicating that this mRNA is subject to negative regulation by one or more pituitary-dependent factors. Continuous GH treatment of the hypophysectomized rats suppressed the expression of mRNA of GSTs Ya1, Yb1 and Yb2 when given as a continuous infusion, but not when given by an intermittent (twice daily) GH-injection schedule. Combination of continuous exposure to GH with thyroxine treatment resulted in a more complete suppression of GSTs Ya1, Yb1 and Yb2. In contrast, thyroxine increased the expression of GST Yc in hypophysectomized rats. These studies establish that several Alpha and Mu class GSTs are expressed in a sex-dependent fashion in adult rat liver, where they are regulated by multiple pituitary-dependent hormones through pretranslational mechanisms.


1970 ◽  
Vol 119 (4) ◽  
pp. 629-634 ◽  
Author(s):  
M. J. Clemens ◽  
A. Korner

1. Incorporation of [14C]leucine into protein in rat liver slices, incubated in vitro, increased as the concentration of unlabelled amino acids in the incubation medium was raised. A plateau of incorporation was reached when the amino acid concentration was 6 times that present in rat plasma. Labelling of RNA by [3H]orotic acid was not stimulated by increased amino acid concentration in the incubation medium. 2. When amino acids were absent from the medium, or present at the normal plasma concentrations, no effect of added growth hormone on labelling of protein or RNA by precursor was observed. 3. When amino acids were present in the medium at 6 times the normal plasma concentrations addition of growth hormone stimulated incorporation of the appropriate labelled precursor into protein of liver slices from normal rats by 31%, and into RNA by 22%. A significant effect was seen at a hormone concentration as low as 10ng/ml. 4. Under the same conditions addition of growth hormone also stimulated protein labelling in liver slices from hypophysectomized rats. Tissue from hypophysectomized rats previously treated with growth hormone did not respond to growth hormone in vitro. 5. No effect of the hormone on the rate or extent of uptake of radioactive precursors into acid-soluble pools was found. 6. Cycloheximide completely abolished the hormone-induced increment in labelling of both RNA and protein. 7. It was concluded that, in the presence of an abundant amino acid supply, growth hormone can stimulate the synthesis of protein in rat liver slices by a mechanism that is more sensitive to cycloheximide than is the basal protein synthesis. The stimulation of RNA labelling observed in the presence of growth hormone may be a secondary consequence of the hormonal effect on protein synthesis. 8. The mechanism of action of growth hormone on liver protein synthesis in vitro was concluded to be similar to its mechanism of action in vivo.


1985 ◽  
Vol 104 (3) ◽  
pp. 433-439 ◽  
Author(s):  
W. M. Moseley ◽  
L. F. Krabill ◽  
A. R. Friedman ◽  
R. F. Olsen

ABSTRACT Serum GH concentrations in steers were examined during extended treatment with synthetic GH-releasing factor(1–44)NH2 (GRF). The results indicate that GRF given as frequent microinjections stimulate and sustain raised serum GH concentrations for at least 5 days in steers. The GH secretory pattern remained episodic and was characterized by a significant increase in the amplitude of the GH pulses without a change in the number of GH pulses per day. In the first of two experiments, young Holstein steers received 0, 0·05, 0·5 or 5·0 mg GRF during a 24-h period as microinjections every 3·75 min. The 5·0 mg GRF/24 h dose significantly increased baseline GH, amplitude of GH pulses and area under the GH curve compared with the other treatments. The number of GH pulses/24 h was similar for all doses of GRF. In a second experiment with Holstein steers, administration of 3·6 mg GRF/day for 5 days increased serum GH concentrations throughout the duration of the treatment without altering the temporal GH secretory pattern. The GH response to GRF did not diminish from days 1 to 5 of treatment suggesting that there was no pituitary desensitization. J. Endocr. (1985) 104, 433–439


1983 ◽  
Vol 37 (6) ◽  
pp. 473-475 ◽  
Author(s):  
Susan N. Perkins ◽  
William S. Evans ◽  
Michael O. Thorner ◽  
Michael.J. Cronin

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