Age-related release of prolactin by the pituitary and the pituitary-hypothalamic complex in vitro: an attempt to describe the development of the hypothalamic prolactin-inhibiting and -releasing activities in male rats

1987 ◽  
Vol 115 (3) ◽  
pp. 405-409 ◽  
Author(s):  
S. Karanth ◽  
A. Dutt ◽  
H. S. Juneja

ABSTRACT We have recently demonstrated that the pituitary hypothalamic complex (PHC) is a good model for studying interactions between the hypothalamus and pituitary in vitro. The amount of prolactin secreted by the PHC is an index of prolactin secreted by the pituitary in the presence of hypothalamic control, while the amount released by the whole pituitary alone is an index of prolactin secreted in the absence of hypothalamic control. The amount of prolactin secreted by the PHC has been regarded as an index of hypothalamic prolactin-releasing activity (HPRA), while the difference in the amounts of prolactin secreted by the whole pituitary and the PHC is the hypothalamic prolactin-inhibiting activity (HPIA). Attempts were made to correlate HPRA and HPIA to the development of serum concentrations of prolactin from days 7 to 77 in male rats. The HPRA increased steadily from days 7 to 56, decreased significantly on day 63 and thereafter remained unchanged until day 77. The HPIA was low on days 7 and 14 and increased steadily up to day 49, with no further significant variations. The developmental patterns of HPRA and HPIA were comparable up to day 49. Serum concentrations of prolactin increased significantly until day 28 and remained fairly constant until day 49. The weight of the pituitary gland increased from 1·0± 0·03 mg (mean ± s.e.m.) on day 7 to 7·76 ± 0·32 mg on day 63 and remained unchanged thereafter. The weight of the hypothalamic islet was 31·5 ± 2·88 mg on day 7, 34·83 ±1·45 mg on day 14 and 50·4 ± 4·01 mg on day 21. After day 21 the weights of the hypothalamic islets were not significantly altered, except on day 49. It was concluded that serum concentrations of prolactin are regulated by interaction or competition between HPRA and HPIA at the level of the pituitary. J. Endocr. (1987) 115, 405–409

1977 ◽  
Vol 232 (6) ◽  
pp. E580
Author(s):  
M P Zabinski ◽  
P Biancani

Longitudinal force-length relationship of the rat esophagus was studied in vitro in three age groups: 1 mo, 3 mo, and 12 mo. The length of maximum force development (MFD) occurs at 1.4-1.5 times the in vivo length for all age groups. The active force developed at MFD increases markedly with age. The difference in the active forces in the 3-mo and 12-mo age groups is due to differences in cross section because the active stress of the esophagus in the longitudinal direction is approximately equal for the two age groups. The active stress in the 1-mo-old rats is lower than in the 3-mo-old rats, suggesting an increased contractility of the esophagus with age in this period of development.


1977 ◽  
Vol 86 (4) ◽  
pp. 728-732 ◽  
Author(s):  
Y. Epstein ◽  
B. Lunenfeld ◽  
Z. Kraiem

ABSTRACT The aim of this study was to investigate effects of androgens on gonadotrophin release in response to gonadotrophin-releasing hormone (Gn-RH) stimulation in vitro. Hemipituitaries of mature male rats were pre-incubated for 90 min with T, DHT, 3α- or 3β-diol (4 ng or 4 μg/ml medium), and the incubation continued for 240 min after adding Gn-RH (1 ng/ml medium). Gn-RH caused a 4-5-fold rise in the secretion of LH and a 2-fold rise in FSH secretion. The effect of the androgens was dose-dependent. At low levels, T and DHT exerted no effect on Gn-RH-stimulated gonadotrophin release, whereas the two androstanediols (3α- and 3β-diol) augmented the Gn-RH stimulation of both gonadotrophins, though preferentially LH. With high doses of androgens, the results obtained showed: a) no effect of T; b) DHT suppression of the Gn-RH-stimulated FSH release; c) suppression of Gn-RH stimulation by 3α- and 3β-diol regarding both LH and FSH. It is concluded that T exerts through its reduced metabolites a feedback effect on the pituitary gland responsiveness to Gn-RH stimulation.


2012 ◽  
Vol 302 (3) ◽  
pp. H560-H566 ◽  
Author(s):  
Lori S. Kang ◽  
Timothy R. Nurkiewicz ◽  
Guoyao Wu ◽  
Matthew A. Boegehold

Nitric oxide (NO) mediates a major portion of arteriolar endothelium-dependent dilation in adults, but indirect evidence has suggested that NO contributes minimally to these responses in the young. Isolated segments of arterioles were studied in vitro to verify this age-related increase in NO release and investigate the mechanism by which it occurs. Directly measured NO release induced by ACh or the Ca2+ ionophore A-23187 was five- to sixfold higher in gracilis muscle arterioles from 42- to 46-day-old (juvenile) rats than in those from 25- to 28-day-old (weanling) rats. There were no differences between groups in arteriolar endothelial NO synthase (eNOS) expression or tetrahydrobiopterin levels, and arteriolar l-arginine levels were lower in juvenile vessels than in weanling vessels (104 ± 6 vs.126 ± 3 pmol/mg). In contrast, agonist-induced eNOS Thr495 dephosphorylation and eNOS Ser1177 phosphorylation (events required for maximal activity) were up to 30% and 65% greater, respectively, in juvenile vessels. Juvenile vessels did not show increased expression of enzymes that mediate these events [protein phosphatases 1 and 2A and PKA and PKB (Akt)] or heat shock protein 90, which facilitates Ser1177 phosphorylation. However, agonist-induced colocalization of heat shock protein 90 with eNOS was 34–66% greater in juvenile vessels than in weanling vessels, and abolition of this difference with geldanamycin also abolished the difference in Ser1177 phosphorylation between groups. These findings suggest that growth-related increases in arteriolar NO bioavailability may be due at least partially to changes in the regulation of eNOS phosphorylation and increased signaling activity, with no change in the abundance of eNOS signaling proteins.


1987 ◽  
Vol 116 (1) ◽  
pp. 138-144 ◽  
Author(s):  
Dorothy I. Shulman ◽  
Margaret Sweetland ◽  
Gregory Duckett ◽  
Allen W. Root

Abstract. The GH secretory response to varying doses (15, 30, 60 μg/kg) of sc administered hGHRH 1–44 (or normal saline) was measured in vivo in 10, 20, 30, 40, 50, 60 and 130 days old pentobarbital-anaesthetized, male rats. The 10-min GH level and ΔGH were in general significantly greater in older rats (50, 60, 130 days old) than in younger rats (10, 20 days old) following all doses hGHRH. Ten-day-old animals had no significant GH response to any dose of hGHRH tested. ΔGH correlated significantly with age (r = 0.36; P < 0.0001) and Sm-C level (r = 0.29; P < 0.01) but not with serum testosterone concentrations. Monolayer pituitary cell cultures were established in rats aged 10 to 130 days and were incubated with varying concentrations of hGHRH 1–44 (0.05, 0.5, 5.0, 50 nmol/l or incubation medium). Cultures from 10- and 20-day-old animals had a greater percentage increase over basal GH secretion than other groups at all concentrations of hGHRH tested (P < 0.05). Age-related differences in the GH secretory response to hGHRH are present in male rats from 10 to 130 days. The in vitro results reported here suggest that the increase in magnitude and sensitivity of the GH response to hGHRH observed in pubertal animals in vivo under pentobarbital anaesthesia is likely due to influences above the level of the somatotrope receptor.


1985 ◽  
Vol 105 (2) ◽  
pp. 211-218 ◽  
Author(s):  
B. A. Keel ◽  
T. O. Abney

ABSTRACT The influence of age on the sensitivity of the testis to oestrogens was investigated. Intact male rats at 10, 25, 40 and 53 days of age were injected s.c. with vehicle, 5 or 50 μg oestradiol or diethylstilboestrol (DES)/100 g body wt twice daily for 2 days; the animals were killed 12 h after the last injection. Subsequently, the concentrations of testicular androgens and serum LH, prolactin, testosterone and androstanediol (5α-androstane-3α, 17β-diol) were measured. Testicular androgen production was determined in vitro in the presence or absence of human chorionic gonadotrophin (hCG) or dibutyryl cyclic AMP (dbcAMP). Androgens in the serum and testes displayed an age-related alternating pattern with androstanediol being the major androgen produced at 27 days of age. As a result of oestrogen treatment, serum LH concentrations were decreased while serum prolactin was increased. Serum testosterone was decreased by 36–55% in the 12-day-old group and further reduced by 95% of control values by day 55; serum androstanediol was less sensitive to oestrogen suppression. Testicular concentrations of both testosterone and androstanediol exhibited a marked reduction in 12-day-old animals as a result of oestrogen administration. These values were reduced by 85–95% at day 27 and remained suppressed even at 55 days. Basal production of testosterone was unaffected by oestrogen treatment in 12- and 27-day-old animals but was markedly decreased by day 42. Significant suppression of basal production of androstanediol was observed as early as day 12. Oestradiol treatment caused a significant reduction in hCG responsiveness of both androgens at days 12, 42 and 55. Oestrogen administration resulted in a significant (32–59%) decline in dbcAMP-responsive testosterone production in the 42-day group and a further suppression in the 55-day group. A marked inhibition of dbcAMP-stimulated androstanediol production was also observed in the 42- and 55-day groups. Testosterone production in response to dbcAMP was not significantly altered in the 12- and 27-day groups. With few exceptions the effects of oestradiol and DES on testicular function were similar. The data presented here suggest that the inhibitory effects of oestrogens become more pronounced as the animal approaches adulthood, that oestradiol and DES are similarly effective in regulating testicular function at all ages studied and that the production of both testosterone and androstanediol are suppressed by oestrogen administration. J. Endocr. (1985) 105, 211–218


Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 859-864 ◽  
Author(s):  
Meghan M. Taylor ◽  
Sara L. Bagley ◽  
Willis K. Samson

Intermedin (IMD), a novel member of the adrenomedullin (AM), calcitonin gene-related peptide (CGRP), amylin (AMY) peptide family, has been reported to act promiscuously at all the known receptors for these peptides. Like AM and CGRP, IMD acts in the circulation to decrease blood pressure and in the brain to inhibit food intake, effects that could be explained by activation of the known CGRP, AM, or AMY receptors. Because AM, CGRP, and AMY have been reported to affect hormone secretion from the anterior pituitary gland, we examined the effects of IMD on GH, ACTH, and prolactin secretion from dispersed anterior pituitary cells harvested from adult male rats. IMD, in log molar concentrations ranging from 1.0 pm to 100 nm, failed to significantly alter basal release of the three hormones. Similarly, IMD failed to significantly alter CRH-stimulated ACTH or TRH-stimulated prolactin secretion in vitro. However, IMD concentration-dependently inhibited GHRH-stimulated GH release from these cell cultures. The effects of IMD, although requiring higher concentrations, were as efficacious as those of somatostatin and, like somatostatin, may be mediated, at least in part, by decreasing cAMP accumulation. These actions of IMD were not shared by other members of the AM-CGRP-AMY family of peptides, suggesting the presence of a novel, unique IMD receptor in the anterior pituitary gland and a potential neuroendocrine action of IMD to interact with the hypothalamic mechanisms controlling growth and metabolism.


2000 ◽  
Vol 166 (3) ◽  
pp. 669-675 ◽  
Author(s):  
LC Gonzalez ◽  
L Pinilla ◽  
M Tena-Sempere ◽  
E Aguilar

The secretion of PRL is controlled by different hypothalamic signals. Depending on the experimental model, PRL secretion increases or decreases after activation of N-methyl-d -aspartic acid and kainate receptors. Recently we have described that activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors inhibits PRL secretion in prepubertal male rats. The aim of present study was to examine (1) the physiological relevance of this finding, (2) the possible age-related changes observed after activation or blockade of AMPA receptors, (3) the specificity of the AMPA effect, (4) the hypothalamic and/or pituitary localization of AMPA action, and (5) the mechanism(s) of action of AMPA agonists. In a first set of experiments, neonatal males (5 and 10 days old) and prepubertal (23 days old) male rats were injected with AMPA (1, 2.5 or 5 mg/kg) or the antagonist of AMPA receptors 1,2,3, 4-tetrahydro-6-nitro-2,3-dioxo-! benzo (f) quinoxaline-7-sulfonamide (NBQX; 0.25 or 0.50 mg/kg). Serum PRL concentrations decreased significantly 15 and 30 min after i.p. administration of AMPA in prepubertal male rats, while the inhibitory effect of AMPA was not observed in 5- and 10-day-old males. The effect of AMPA was abolished by NBQX but not by MK-801 (a selective antagonist of NMDA receptors). NBQX alone (0.25 or 0.50 mg/kg) had no effect on PRL release. In vitro, AMPA slightly stimulated PRL secretion by hemipituitaries from prepubertal males, suggesting that the hypothalamus is likely the site of action for the reported inhibitory action of AMPA on PRL release. In this sense, the blockade of AMPA effects in animals pretreated with domperidone (a dopaminergic antagonist) or alpha-methyl-p-tyrosine (an inhibitor of dopamine synthesis) suggests that an increase in the release of hypothalamic dopamine is probably the mechanism i! nvolved in the effect of AMPA. In a second set of experiments, the effects of AMPA (2.5 mg/kg i.p.) and NBQX (0.5 mg/kg i.p. and 20 or 40 nmol i.c.v.) were tested in freely moving adult male rats sampled during periods of 2, 3 or 6 h. In contrast with data obtained in prepubertal rats, neither AMPA nor NBQX affected PRL secretion. In conclusion, these data indicate that activation of AMPA receptors inhibits PRL secretion in prepubertal male rats. This effect probably involves the release of dopamine from the hypothalamus and disappears in adulthood.


1982 ◽  
Vol 208 (3) ◽  
pp. 695-701 ◽  
Author(s):  
C A Tate ◽  
P E Wolkowicz ◽  
J McMillin-Wood

In order to examine the effect of a single bout of exercise on hepatic mitochondrial function, starved untrained male rats swam at 34-35 degrees C with a tail weight (5% of body wt.) for 100 min. The rates of ADP-stimulated and uncoupled respiration were higher in the mitochondria isolated from the exercised rats regardless of the substrate utilized. Succinate-linked Ca2+ uptake was 48% greater in the exercised group; however, Ca2+ efflux was markedly depressed. The inhibition of Ca2+ uptake by Mg2+ was higher in the control group, so that the difference in Ca2+ uptake between the two groups was greater in the presence of Mg2+ than in its absence. The response of phosphorylating respiration and Ca2+ fluxes to exogenous phosphate and the pH of the assay medium differed in the exercise group. These observations with the exercised group were not related to non-specific stress. The exercise-induced mitochondrial-functional alterations are reminiscent of those obtained from mitochondria isolated from glucagon- or catecholamine-treated sedentary rats. Thus, adrenergic stimulation as well as other factors may be operating during exercise, leading to an alteration of mitochondrial function in vitro.


Sign in / Sign up

Export Citation Format

Share Document