RESPONSES OF RAT FETAL ADRENALS TO SYNTHETIC ADRENOCORTICOTROPHIC HORMONE AND α-MELANOCYTE-STIMULATING HORMONE: IN-VIVO AND IN-VITRO STUDIES

1982 ◽  
Vol 92 (1) ◽  
pp. 23-30 ◽  
Author(s):  
J. P. DUPOUY
Keyword(s):  
Physiological Role ◽  
Female Rats ◽  
Fetal Life ◽  
Melanocyte Stimulating Hormone ◽  
Pituitary Glands ◽  
High Doses ◽  
And Function ◽  
Stimulating Hormone

The response of the adrenals from rat fetuses at 16,18 and 20 days of gestation to 1–24 ACTH and α-melanocyte-stimulating hormone (α-MSH) was studied in vitro. The response to 1–24 ACTH increased as gestation progressed. By the end of fetal life, corticosterone release induced by ACTH from whole adrenals was greater than that observed with adrenal tissue from non-pregnant adult female rats. High doses of α-MSH also stimulated adrenal activity but the response to ACTH was always higher than that to α-MSH. The effect of 1–24 ACTH and α-MSH on fetal adrenal growth was also compared in vivo. The adrenal atrophy induced by fetal hypophysectomy on day 17 of gestation could be prevented by i.m. administration of 10 μg 1–24 ACTH or α-MSH. However, the adrenal growth was greater in ACTH-treated fetuses than in α-MSH-treated ones. Later in gestation, between days 19 and 20, 1–24 ACTH but not α-MSH was able to prevent atrophy induced by fetal hypophysectomy. These findings are discussed in relation to the literature on levels of ACTH and α-MSH in the plasma and pituitary glands of the rat throughout the last third of gestation. High levels of ACTH in the fetal circulation contrast sharply with very weak or undetectable concentrations of α-MSH. Since the present data suggest that both trophic and steroidogenic activities of ACTH were greater than those of α-MSH, it may be concluded that ACTH but not α-MSH plays a major physiological role during gestation in the regulation of both fetal adrenal growth and function in the rat.

scholarly journals α-Melanocyte Stimulating Hormone Prevents Lipopolysaccharide-Induced Vasculitis by Down-Regulating Endothelial Cell Adhesion Molecule Expression

Endocrinology ◽  
2003 ◽  
Vol 144 (1) ◽  
pp. 360-370 ◽  
Author(s):  
T. E. Scholzen ◽  
C. Sunderkötter ◽  
D.-H. Kalden ◽  
T. Brzoska ◽  
M. Fastrich ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Inflammatory Diseases ◽  
Nuclear Factor Κb ◽  
Vascular Damage ◽  
Adhesion Assay ◽  
Melanocyte Stimulating Hormone ◽  
And Function ◽  
Stimulating Hormone

Abstract The neuroendocrine hormone α-melanocyte stimulating hormone (MSH) has profound antiinflammatory and immunomodulating properties. Here we have examined the possibility that α-MSH may interfere with the expression and function of cell adhesion molecules (CAMs) expressed by human dermal microvascular endothelial cells (HDMECs) in response to lipopolysaccharide (LPS) or TNFα in vitro and in vivo. In HDMEC, α-MSH (10−8/10−12m) profoundly reduced the mRNA and protein expression of E-selectin, vascular CAM (VCAM)-1, and intercellular CAM (ICAM)-1 induced by LPS or TNFα as determined by semiquantitative RT-PCR, ELISA, and fluorescence-activated cell sorter analysis. In addition, α-MSH significantly impaired the LPS-induced ICAM-1 and VCAM-1-mediated adhesion of lymphocytes to HDMEC monolayer in a functional adhesion assay. Likewise, α-MSH effectively inhibited the transcription factor nuclear factor-κB activation in HDMEC, which is required for CAM gene expression. Importantly in vivo, in murine LPS-induced cutaneous vasculitis (local Shwartzman reaction), a single ip injection of α-MSH significantly suppressed the deleterious vascular damage and hemorrhage by inhibiting the sustained expression of vascular E-selectin and VCAM-1. This persistent expression has been implicated in the dysregulation of diapedesis and activation of leukocytes, which subsequently leads to hemorrhagic vascular damage. Our findings indicate that α-MSH may have an important therapeutical potential for the treatment of vasculitis, sepsis, and inflammatory diseases.

DIFFERENCES IN THE RELEASE OF MELANOCYTE-STIMULATING HORMONE IN VITRO BY RAT PITUITARY GLANDS COLLECTED AT VARIOUS TIMES DURING THE OESTROUS CYCLE

1978 ◽  
Vol 78 (1) ◽  
pp. 1-6 ◽  
Author(s):  
ADRIANA VIVAS ◽  
MARÍA ESTER CELIS
Keyword(s):  
Pituitary Gland ◽  
Oestrous Cycle ◽  
Biological Assay ◽  
Melanocyte Stimulating Hormone ◽  
Pituitary Tissue ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Stimulating Hormone

The release of melanocyte-stimulating hormone (MSH) into the medium during incubation and the pituitary tissue content of MSH were measured separately using pituitary glands collected from rats at various stages of the oestrous cycle. The MSH was measured by a biological assay using a synthetic α-MSH as standard. The release of MSH was maximal during the pro-oestrous phase and MSH content of the pituitary gland was highest during dioestrus. The influences of the tripeptide Pro-Leu-Gly-NH2, which inhibits MSH secretion in vivo, and of progesterone on the release of MSH in vitro were studied with tissue collected at various phases of the oestrous cycle. Pro-Leu-Gly-NH2 was effective in inhibiting MSH release both at pro-oestrus and oestrus but not at dioestrus. Progesterone overcame this inhibition.

scholarly journals Inhibition of salmon calcitonin on secretion of progesterone and GnRH-stimulated pituitary luteinizing hormone

1999 ◽  
Vol 277 (1) ◽  
pp. E49-E55 ◽  
Author(s):  
Shiow-Chwen Tsai ◽  
Chien-Chen Lu ◽  
Jiann-Jong Chen ◽  
Yu-Chung Chiao ◽  
Shyi-Wu Wang ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Granulosa Cells ◽  
Salmon Calcitonin ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Progesterone Production ◽  
Ovx Rats ◽  
Pituitary Glands

The effects of salmon calcitonin (sCT) on the production of progesterone and secretion of luteinizing hormone (LH) were examined in female rats. Diestrous rats were intravenously injected with saline, sCT, human chorionic gonadotropin (hCG), or hCG plus sCT. Ovariectomized (Ovx) rats were injected with saline or sCT. In the in vitro experiments, granulosa cells and anterior pituitary glands (APs) were incubated with the tested drugs. Plasma LH levels of Ovx rats were reduced by sCT injection. Administration of sCT decreased the basal and hCG-stimulated progesterone release in vivo and in vitro. 8-Bromo-cAMP dose dependently increased progesterone production but did not alter the inhibitory effect of sCT. H-89 did not potentiate the inhibitory effect of sCT. Higher doses of 25-hydroxycholesterol and pregnenolone stimulated progesterone production and diminished the inhibitory effects of sCT. sCT did not decrease basal release of LH by APs, but pretreatment of sCT decreased gonadotropin-releasing hormone (GnRH)-stimulated LH secretion. These results suggested that sCT inhibits progesterone production in rats by preventing the stimulatory effect of GnRH on LH release in rat APs and acting directly on ovarian granulosa cells to decrease the activities of post-cAMP pathway and steroidogenic enzymes.

GONADOTROPHIN RELEASE IN VITRO, IN THE PRESENCE AND ABSENCE OF LUTEINIZING HORMONE RELEASING HORMONE, BY PITUITARY GLANDS FROM OVARIECTOMIZED AND SHAM-OPERATED IMMATURE FEMALE RATS OF VARIOUS AGES

1981 ◽  
Vol 88 (3) ◽  
pp. 375-379
Author(s):  
J. DULLAART
Keyword(s):  
Female Rats ◽  
Ovariectomized Rats ◽  
Immature Female ◽  
Releasing Hormone ◽  
Incubation Experiments ◽  
Immature Rats ◽  
Pituitary Glands ◽  
Lh Releasing Hormone

Hemipituitary glands of immature female rats, aged 10, 15, 20, 25, 30 and 35 days and either ovariectomized or sham-operated 5 days earlier, were incubated for 2 h in vitro with or without LH releasing hormone. Concentrations of LH and FSH were determined at the end of the incubations in the incubation media and in the hemipituitary glands, and also in the sera collected at the beginning of the incubation experiments. Results showed that in many instances gonadotrophin release was higher after incubation of glands of ovariectomized rats than with glands of control animals. However, these effects of ovariectomy were much smaller than those observed in vivo and were generally absent in rats of less than 20 days of age. It was concluded that ovariectomy may change the secretory characteristics of the gonadotrophic cells of immature rats but that such changes were largely restricted to immature rats older than 20 days.

Effects of different opiate agonists on melanocyte-stimulating hormone release: in vivo and in vitro studies

1980 ◽  
Vol 58 (3) ◽  
pp. 326-329 ◽  
Author(s):  
M. E. Celis
Keyword(s):  
Opioid Peptides ◽  
In Vitro Studies ◽  
Hormone Release ◽  
Low Concentration ◽  
Melanocyte Stimulating Hormone ◽  
Dose Dependent ◽  
Stimulating Hormone

The effects of Leu-enkephalin, Met-enkephalin, and β-endorphin on melanocyte-stimulating hormone (MSH) secretion were studied in vivo and in vitro. The three opioid peptides release MSH. In vitro this release is dose dependent for Met-enkephalin between 10 and 1000 ng/mL and for Leu-enkephalin between 10 and 100 ng/mL. β-Endorphin releases MSH at the low concentration of 1 ng/mL and the effect is dose dependent between 1 and 100 ng/mL. Naloxone reverses this effect. In vivo the three petptides release MSH.

Three types of alpha-melanocyte-stimulating hormone: bioactivities and half-lives

1983 ◽  
Vol 245 (1) ◽  
pp. E47-E54 ◽  
Author(s):  
D. Rudman ◽  
B. M. Hollins ◽  
M. H. Kutner ◽  
S. D. Moffitt ◽  
M. J. Lynn
Keyword(s):  
Tissue Slices ◽  
Melanocyte Stimulating Hormone ◽  
Lipolytic Action ◽  
Acetyl Group ◽  
Isolated Adipocytes ◽  
Hydroxy Groups ◽  
Kinetics Of ◽  
Stimulating Hormone

Three types of alpha-melanocyte-stimulating hormone (alpha MSH) that differ in the acetyl status of the N-terminal serine have been found in the neurointermediate lobe of the pituitary gland and in the brain: desacetyl alpha MSH, which lacks an acetyl group; monoacetyl alpha MSH, in which the amino group of the serine is acetylated; and diacetyl alpha MSH, in which both amino and hydroxy groups of the serine are acetylated. We compared the lipolytic and melanotropic actions of these three peptides, and their rates of disappearance from plasma, both in vitro and in vivo. The following differences were found. a) For in vitro lipolytic actions on rabbit adipose tissue slices, the potencies differed according to the order diacetyl = monoacetyl greater than desacetyl. On rabbit isolated adipocytes, however, the three peptides were equipotent. b) For in vivo lipolytic action in the rabbit, not only potency but also kinetics differed. Diacetyl alpha MSH had the slowest onset, longest duration, and greatest potency. The desacetyl variant had the quickest onset, shortest duration, and least potency. c) The half-life for elimination from rabbit plasma both in vitro and in vivo was shortest for the desacetyl form and longest for the diacetyl peptide. d) For in vitro melanotropic effect on frog skin, kinetics of action were the same for all three peptides, but potency differed according to the order diacetyl = monoacetyl greater than desacetyl. Thus acetylation of alpha MSH alters lipolytic and melanotropic potencies in vitro and lipolytic potency and kinetics in vivo. These differences result in part from the fact that acetylation slows the degradation of the tridecapeptide both inside and outside the circulation.

MELANOCYTE STIMULATING HORMONE INHIBITION BY ACETYLCHOLINE AND NORADRENALINE IN THE FROG SKIN BIOASSAY

1966 ◽  
Vol 51 (1) ◽  
pp. 149-160 ◽  
Author(s):  
Halvor Möller ◽  
Aaron B. Lerner
Keyword(s):  
Frog Skin ◽  
Rana Pipiens ◽  
Individual Response ◽  
Melanocyte Stimulating Hormone ◽  
Skin Samples ◽  
Stimulating Hormone

ABSTRACT The mechanism of aggregation induced in MSH-dispersed dermal melanocytes was studied in Rana pipiens by reflectance photometry in vitro and by microscopy in vivo. Acetylcholine inhibits MSH strongly and irreversibly in one third of all frogs tested in vitro and has almost no effect on the remaining animals. No lightening action occurs in vivo. Different skin samples from the same animal give the same response to acetylcholine. An individual response to acetylcholine implies similar responses to other cholinergics. The lightening action of acetylcholine is inhibited by atropine. Noradrenaline induces a reversible MSH-inhibition in all frogs in vitro as well as in vivo. The lightening action of noradrenaline, inhibited by sympatholytics, is ten times stronger than that of acetylcholine. The l-isomer has only twice the lightening potency as the d-isomer. Both lightening agents work if given at the maximum of MSH-dispersion or before the addition of MSH. Fundamental differences between the mechanisms of dispersion and aggregation, and between the lightening induced by acetylcholine and by noradrenaline, are emphasized.

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