Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

1990 ◽  
Vol 127 (3) ◽  
pp. 417-425 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan ◽  
D. Attardo
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Recombinant Dna ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Caudal Lobe ◽  
Direct Inhibitory Effect ◽  
Pituitary Glands

ABSTRACT Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1–100 μg/kg. In-vitro preincubation of chicken pituitary glands for 0·5–4·0 h with 0·1 μmol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0·1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulati concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h. Pituitary binding sites for 125I-[Tyr1]-SRIF were not affected by pretreatment of pituitary glands for 2–12 h in vitro with thyroxine or oestradiol-17β (1 nmol/l–10 μmol/l) or with ovine GH or recombinant DNA-derived chicken GH (1–100 μg/ml in vitro and 100–1000 μg/kg in vivo). Ovine prolactin, at concentrations of 1–100 μg/ml was also without effect on 125I-[Tyr1]-SRIF binding to pituitary membranes following a 2- or 4-h incubation with pituitary glands. Pituitary binding sites for 125I-[Tyr1]-SRIF were, however, increased after a 24-h incubation with 1 μmol tri-iodothyronine (T3)/l in vitro and 4 and 24 h after the administration of T3 (100–1000 μg/kg) in vivo. Although T3 had no direct inhibitory effect on 125I-[Tyr1]-SRIF binding to pituitary membranes, binding was suppressed 1 and 2 h after the in-vivo administration of T3 at concentrations of 100–1000 μg/kg. These results therefore demonstrate homologous and heterologous regulation of SRIF-binding sites in the chicken pituitary gland. Journal of Endocrinology (1990) 127, 417–425

In-vivo and in-vitro secretion of prolactin by lactating rat adenohypophyses as a function of intracellular age

1984 ◽  
Vol 101 (1) ◽  
pp. 27-32 ◽  
Author(s):  
F. Mena ◽  
G. Martínez-Escalera ◽  
C. Clapp ◽  
C. E. Grosvenor
Keyword(s):  
Pituitary Gland ◽  
Incubation Period ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Polyacrylamide Gel ◽  
Pituitary Glands ◽  
H 26

ABSTRACT Adenohypophysial prolactin of lactating rats was pulse-labelled by [3H]leucine injected i.v. at the time of removal of the pups. The [3H]prolactin concentration in the pituitary gland, analysed by polyacrylamide-gel electrophoresis, progressively fell as the time from labelling to removal of the pituitary gland increased from 8 to 24 h, which suggests that there was a loss of hormone as it aged within the gland. Suckling effectively provoked the depletion–transformation of total and [3H]prolactin (extracted at pH 7·2) when applied after 8 h but not when applied after either 16 or 24 h after removing the pups. In rats whose pups were removed for 8 h, suckling also depleted–transformed [3H]prolactin labelled 4 h, but not that labelled 1 h before suckling. The pituitary glands of other lactating rats were labelled with [3H]leucine injected i.v. at various times before removing the glands and incubating them in medium 199. The secretion into the medium of [3H]prolactin labelled either 4, 8, 16 or 24 h beforehand was maximal during the first 30 min then declined from 30 to 240 min of incubation. However, secretion of prolactin labelled 1 h and 10 min beforehand reached a maximum after 0·5–1 h and 2 h of incubation respectively, then remained constant during the remainder of the 4-h incubation period. The total 4-h secretion of [3H]prolactin was greatest (65% of preincubation concentration) from those glands labelled 4 h before in contrast to those labelled 10 min (15%) or 1 (38%), 8 (34%), 16 (18%) or 24 h (26%) before incubation. Taken together, these data suggest that prolactin synthesized 4 h earlier is more likely to be released in response to physiological stimuli than is more recently formed prolactin or prolactin which has remained in the pituitary gland for 16 h or longer. J. Endocr. (1984) 101, 27–32

Role of endothelial cells in regulating hemoglobin-induced changes in lymphatic pumping

1992 ◽  
Vol 263 (6) ◽  
pp. H1880-H1887 ◽  
Author(s):  
R. M. Elias ◽  
J. Eisenhoffer ◽  
M. G. Johnston
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Inhibitory Effect ◽  
Direct Inhibitory Effect ◽  
Induced Changes ◽  
Lymphatic Pumping ◽  
Pumping Activity

Studies with a sheep isolated duct preparation in vivo demonstrated that the route of administration of hemoglobin was important in demonstrating its inhibitory effect on lymphatic pumping. With autologous oxyhemoglobin administered intravenously (final plasma concentration 5 x 10(-5) M), pumping was not inhibited. However, the addition of oxyhemoglobin (5 x 10(-5) M) into the reservoir (lumen of the duct) resulted in > 95% inhibition of pumping. The extraluminal administration of oxyhemoglobin (10(-5) M) to bovine mesenteric lymphatics in vitro resulted in a 40% inhibition of pumping, whereas the introduction of oxyhemoglobin (10(-5) M) into the lumen of the vessels suppressed pumping 95%. In vessels mechanically denuded of endothelium, intraluminal oxyhemoglobin inhibited pumping 50%. These results suggested that oxyhemoglobin depressed pumping through an effect on both smooth muscle and endothelium. Once pumping was inhibited with oxyhemoglobin administration, stimulation of the duct with elevations in transmural pressure restored pumping activity when endothelial cells were present. However, in the absence of endothelium, pumping decreased with increases in distending pressures. We conclude that oxyhemoglobin has a direct inhibitory effect on lymphatic smooth muscle. The ability of oxyhemoglobin to alter the pressure range over which the lymph pump operates appears to be dependent on an intact endothelium.

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.

The effect of the somatostatin analog SMS 201-995 on normal growth hormone secretion in the rat.

1987 ◽  
Vol 115 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Steven W. J. Lamberts ◽  
Theo Verleun ◽  
Joke M. Zuiderwijk ◽  
Rob Oosterom
Keyword(s):  
Dopamine Agonist ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Inhibitory Effect ◽  
Somatostatin Analog ◽  
Pituitary Tumours ◽  
Pituitary Glands

Abstract. The somatostatin analog SMS 201-995 was recently shown to be effective in suppressing GH secretion and in causing tumour shrinkage in patients with GH-secreting pituitary tumours. In this respect, the action of SMS 201-995 seems similar to that of the dopamine-agonist bromocriptine in patients with PRL-secreting pituitary tumours. In the present study we compared the respective effects of SMS 201-995 and bromocriptine on normal rat GH and PRL release in vivo and in vitro. Both in vitro and in vivo, repeated administration of SMS for up till 6 days suppressed circulating GH concentrations, and the ability of the pituitary glands to release GH in vitro. A dose-dependent diminution occurred of the total pituitary GH content in rats treated in vivo with SMS 201-995 for 4–6 days. During short-term in vitro incubation for only 4 h, the total amount of GH measured in the medium + gland was also diminished. Chronic administration with SMS 201-995 (2 μg/kg twice daily for 15 days), however, resulted in a complete desensitization of its inhibitory effect on GH synthesis and release. In similar experiments it was shown that the dopamine agonist bromocriptine affects normal PRL secretion in a different manner. Both in vitro (10 nmol/l) and in vivo administration for 6 days (0.2 mg/kg twice daily) greatly inhibited circulating PRL levels and the ability of the pituitary glands to release PRL in vitro. This is, however, in all instances accompanied by an accumulation of PRL within the pituitary gland. Long-term bromocriptine administration (0.2 mg/kg twice daily for 15 days) inhibited PRL secretion, and finally also a decrease in the total pituitary PRL content was observed. It is shown in this study that SMS 201-995 and bromocriptine affect hormone release by normal pituitary glands in a different manner. SMS 201-995 acutely inhibits GH release and diminishes within a few hours of exposure also the GH content in normal cells by a powerful inhibition of GH synthesis and/or an increase in intracellular degradation of GH. Bromocriptine, however, exerts primarily an inhibitory effect on PRL release, whereas an inhibition of synthesis and/or degradation of intracellular PRL is evident only after long-term exposure to the drug.

Sensitivity of thyrotropin secretion to TSH-releasing hormone in food-restricted rats

1991 ◽  
Vol 124 (2) ◽  
pp. 194-202 ◽  
Author(s):  
Felipe Rodriguez ◽  
Mario Mellado ◽  
Eladio Montoya ◽  
Trinidad Jolin
Keyword(s):  
Plasma Membrane ◽  
Binding Sites ◽  
Food Restriction ◽  
Inhibitory Effect ◽  
Secretion Rate ◽  
Tsh Secretion ◽  
Ad Libitum ◽  
Food Consumed

Abstract. The aim of the present study was to identify the mechanisms involved in the reduction of TSH secretion during prolonged food restriction. The basal TSH secretion rate, the TSH secreted in response to TRH, both in vivo and in vitro, and the TSH, nuclear T3, and plasma membrane TRH binding sites in the pituitary were determined in rats receiving 75% (FR75), 50% (FR50) and 25% (FR25) of the food consumed by the ad libitum fed rats (controls). The basal TSH secretion rate (μg·h−1g·(100 g)−1) in FR75, FR50 and FR25 groups were decreased by 19, 42 and 74% of control values, respectively, whereas the TSH secreted in response to TRH in vivo and in vitro was reduced by 21 and 13% in FR50, and 55 and 44% in FR25, respectively, of the corresponding control values. Food restriction increased the TRH binding sites from 229 in controls to 322, 479 and 521 (fmol/mg protein), in FR75, FR50 and FR25 groups, respectively, whereas the opposite was seen in nuclear T3(controls 862, FR75 841, FR50 342 FR25 233 fmol/mg DNA). Moreover, a decrease in the pituitary TSH concentration was observed in FR50 and FR25 rats. The data suggest that an alteration in the amount of TRH reaching the pituitary gland is probably the main responsible for the low plasma TSH values during food restriction. However, an inhibitory effect at the pituitary level cannot be ruled out.

Thyroidal inhibition of chicken pituitary growth hormone: alterations in secretion and accumulation of newly synthesized hormone

1991 ◽  
Vol 131 (1) ◽  
pp. 39-48 ◽  
Author(s):  
R. J. Denver ◽  
S. Harvey
Keyword(s):  
Thyroid Hormone ◽  
Mammalian Species ◽  
Inhibitory Effect ◽  
Stimulatory Action ◽  
Thyrotrophin Releasing Hormone ◽  
Gh Secretion ◽  
Direct Inhibitory Effect ◽  
Hormone Exposure

ABSTRACT Hypothyroidism reduces GH synthesis and release in several mammalian species, in which thyroid hormone directly stimulates GH gene transcription. In contrast, hypothyroidism stimulates GH secretion in birds, in which thyroid hormone directly inhibits pituitary GH release. We have, therefore, investigated the effects of thyroid status on the accumulation of newly synthesized GH in the pituitaries of 8- to 10-week-old Leghorn cockerels in vitro and in vivo. The incorporation of [35S]methionine into immunoprecipitable GH ([35S] GH) was increased, over a 4-h incubation period, in glands from birds made hypothyroid by injections of methimazole (50 mg/kg day for 10 days) in comparison with glands from vehicle-injected controls. Treatment with tri-iodothyronine (T3, 100 μg/kg per day for 10 days) in vivo did not significantly alter the accumulation of [35S]GH in vitro but did block the release of [35S]GH in response to a GH secretagogue (thyrotrophin-releasing hormone; exposure to 280 nmol/l for 30 min) and reduced immunoassayable pituitary GH content. Pretreatment of glands from euthyroid birds with T3 (100 nmol/l) in vitro (for 20 h) reduced the basal accumulation of [35S]GH as well as that induced by another GH secretagogue (GH-releasing factor; 100 nmol/l) during a 6-h labelling period. These results show that, unlike the generally stimulatory action of thyroid hormone in mammals, in birds, T3 exerts a direct inhibitory effect on the accumulation of newly synthesized pituitary GH. Journal of Endocrinology (1991) 131, 39–48

scholarly journals Opposing roles for Egalitarian and Staufen in transport, anchoring and localization of oskar mRNA in the Drosophila oocyte

PLoS Genetics ◽  
2021 ◽  
Vol 17 (4) ◽  
pp. e1009500
Author(s):  
Sabine Mohr ◽  
Andrew Kenny ◽  
Simon T. Y. Lam ◽  
Miles B. Morgan ◽  
Craig A. Smibert ◽  
...  
Keyword(s):  
Binding Sites ◽  
Inhibitory Effect ◽  
Multiple Roles ◽  
Rna Transport ◽  
Nurse Cells ◽  
Stem Loop ◽  
Stem Loop Structure ◽  
Dependent Inhibition

Localization of oskar mRNA includes two distinct phases: transport from nurse cells to the oocyte, a process typically accompanied by cortical anchoring in the oocyte, followed by posterior localization within the oocyte. Signals within the oskar 3’ UTR directing transport are individually weak, a feature previously hypothesized to facilitate exchange between the different localization machineries. We show that alteration of the SL2a stem-loop structure containing the oskar transport and anchoring signal (TAS) removes an inhibitory effect such that in vitro binding by the RNA transport factor, Egalitarian, is elevated as is in vivo transport from the nurse cells into the oocyte. Cortical anchoring within the oocyte is also enhanced, interfering with posterior localization. We also show that mutation of Staufen recognized structures (SRSs), predicted binding sites for Staufen, disrupts posterior localization of oskar mRNA just as in staufen mutants. Two SRSs in SL2a, one overlapping the Egalitarian binding site, are inferred to mediate Staufen-dependent inhibition of TAS anchoring activity, thereby promoting posterior localization. The other three SRSs in the oskar 3’ UTR are also required for posterior localization, including two located distant from any known transport signal. Staufen, thus, plays multiple roles in localization of oskar mRNA.

Absence of effect of somatostatin on the guinea pig gallbladder

1980 ◽  
Vol 58 (2) ◽  
pp. 179-182 ◽  
Author(s):  
Pierre Poitras ◽  
Tadataka Yamada ◽  
John H. Walsh
Keyword(s):  
Guinea Pig ◽  
Muscle Contraction ◽  
Inhibitory Effect ◽  
Cholecystokinin Octapeptide ◽  
Direct Inhibitory Effect

The effect of somatostatin (GH-RIH) on cholecystokinin octapeptide (OP-CCK) or acetylcholine (ACh) induced contraction of the guinea pig gallbladder was evaluated in vitro. GH-RIH failed to inhibit the muscle contraction induced by OP-CCK or ACh. To correlate with the in vitro results, the effect of GH-RIH on OP-CCK induced contraction of the gallbladder was evaluated in the guinea pig in vivo. GH-RIH did not affect the OP-CCK induced contraction of the gallbladder. Our results suggest that GH-RIH does not have direct inhibitory effect on the contraction of the guinea pig gallbladder induced by OP-CCK or ACh.

CHANGES IN OESTRADIOL-17β BINDING IN THE HYPOTHALAMI AND PITUITARY GLANDS OF PERSISTENTLY INFERTILE EWES PREVIOUSLY EXPOSED TO OESTROGENIC SUBTERRANEAN CLOVER: EVIDENCE OF ALTERATIONS TO OESTRADIOL RECEPTORS

1978 ◽  
Vol 78 (2) ◽  
pp. 171-177 ◽  
Author(s):  
B. Y. TANG ◽  
N. R. ADAMS
Keyword(s):  
Binding Sites ◽  
Association Constant ◽  
Feedback Regulation ◽  
Subterranean Clover ◽  
Pituitary Glands ◽  
Number Of Binding Sites ◽  
And Control ◽  
Apparent Association

SUMMARY The binding of [3H]oestradiol-17β to the hypothalamus and pituitary gland of cloveraffected permanently infertile and control ovariectomized ewes was compared in vivo and in vitro. When [3H]oestradiol-17β was infused into the carotid artery (10 ng/min), the total homogenate and the nuclear and protamine-precipitable cytosol fractions of hypothalami and pituitary glands from clover-affected ewes bound significantly more [3H]oestradiol than those of the controls. Cytoplasmic oestradiol-17β receptors from the pituitary glands of clover-affected ewes showed a significantly lower apparent association constant and a higher number of binding sites/mg protein in vitro. It is suggested that the hypothalami and pituitary glands of ewes made permanently infertile by oestrogenic clover are less sensitive to feedback regulation of oestradiol-17β at physiological levels.

Effects of Dipyridamole and Aspirin on Platelet camp Levels and Prostaglandin Biosynthesis in vivo in Patients with Diabetes Mellitus

1979 ◽  
Author(s):  
L.C. Best ◽  
M.B. McGuire ◽  
J.D. Ward ◽  
T. Holland ◽  
F. E. Preston ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Microvascular Complications ◽  
Inhibitory Effect ◽  
Slight Reduction ◽  
Patients With Diabetes ◽  
Direct Inhibitory Effect ◽  
Pre Treatment

Platelets from diabetics with microvascular complications were shown to have lowered aggregation thresholds to ADP, epinephrine and collagen. They also produced more malonyl dialdehyde (MDA) than normal controls. In eight diabetic subjects, administration of dipyridamole (100mg tds)raised platelet aggregation thresholds and increased cyclic AMP levels, presumably as a result of inhibition of phosphodiesterase activity. It also caused a slight reduction of MDA production. This latter effect could be due to the rise in cyclic AMP, although we have found an apparently direct inhibitory effect to dipyridamole on MDA and thromboxane B2 production by intact platelets and platelet microsomes in vitro. On withdrawal of the drug, platelet cyclic AMP and MDA levels and aggregation thresholds returned toward pre-treatment levels. The administration of aspirin (120) plus dipyridamole markedly inhibited platelet aggregation, particularly in response to arachidonic acid and collagen and strongly inhibited MDA production. However, the rise in platelet cyclic AMP levels produced by dipyridamole alone was not present when aspirin and dipyridamole were given together, Aspirin may influence platelet cyclic AMP metabolism directly or by inhibiting prostacyclin formation. Thus, under appropriate conditions, basal platelet cyclic AMP may provide an index of PGI2 production in vivo.

Sign in / Sign up

Export Citation Format

Share Document