Search PubMed⌕ Search

Biomedical subjects

A Miyake

Publications and source records attributed to A Miyake.

At least 289 records · Page 16Linked to original sources
PubMed1983

Estrogen induces the release of luteinizing hormone-releasing hormone in normal cyclic women.

The plasma concentrations of immunoreactive LRH, LH, and FSH were determined by RIA every 6 h until 72 h after iv administration of conjugated estrogens during the midfollicular phase. The percentage change in LH from the preinjection level showed a biphasic pattern after the injection of conjugated estrogens, i.e. significant suppression (-70%) from 6-42 h after the injection, followed by a rebound increase with a peak (+150%) at 56 h. Plasma FSH after the injection also showed a biphasic pattern. The plasma immunoreactive LRH levels were unchanged until 32 h after the injection, but then increased significantly (P less than 0.02) to 160% of the preinjection level at 42 h and then decreased rapidly. These data indicate that 1) estrogen administration results in increases in plasma immunoreactive LRH and LH, and the peak of plasma LRH precedes that of gonadotropin; and 2) the negative feedback effect of estrogen on gonadotropin secretion may not be mediated through LRH.

Adult↗
PubMed1983

Kinetic study on disappearance of gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide (DN-1417) from plasma using a radioimmunoassay for DN-1417 isobutylamide.

Kinetic study of disappearance of gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide (DN-1417) from human plasma has been performed by a sensitive and specific radioimmunoassay (RIA) using antiserum against DN-1417 isobutylamide. Antibody against N-[2-hydroxy-4-(isobutylcarbamoyl)butyryl]-L-histidyl-L-prolinamide (DN-isobutylamide) did not cross-react with any other TRH-related peptides tested. DN-isobutylamide was radioiodinated with 125I by the chloramine T method and the product had a specific activity of about 160 microCi/microgram. The sensitivity of the RIA was 50 pg per tube, and the intra- and inter-assay coefficients of variation at concentrations of 1-10 ng/ml were 7.0-11.6%. DN-1417 in the plasma was converted to a stable form, DN-isobutylamide, by incubation with isopropanol-isobutylamine at room temperature for 2 h. DN-Isobutylamide was separated from 2-hydroxy-4-carboxybutyryl-L-histidyl-L-prolinamide (DN-COOH) using a SEP-PAKTM C18 cartridge before RIa. The recovery of DN-isobutylamide from plasma was 86.2-98.2%. The half-life, volume of distribution and plasma clearance rate of DN-1417 examined in 6 normal male volunteers by intravenous injection of 500 micrograms DN-1417 citrate were 11.5 +/- 5.6 min in the first phase and 89.5 +/- 33.5 min in the second phase, 25.3 +/- 10.0 liters and 745.8 +/- 278.6 1/d, respectively. These results indicate that RIA of DN-isobutylamide is useful for analysing DN-1417 metabolism in humans.

Adolescent↗
PubMed1983

Sodium induces oxytocin release from superfused rat pituitary.

The effects of various osmotic agents on the release of oxytocin were examined in a superfusion system. Oxytocin was released significantly from the rat pituitary by superfusion with medium of an osmolality of 350 mOsm/kg H2O adjusted with NaCl, regardless of the presence of the rat hypothalamus. Media adjusted to an osmolality of 350 mOsm/kg H2O with sucrose, glucose, urea or mannitol had no effect on oxytocin release from the hypothalamo-pituitary complex. Medium containing excess Na2SO4 induced significant release of oxytocin from the pituitary without the hypothalamus. The administration of tetraethylammonium chloride had no oxytocin secretion. These data suggest that oxytocin release from the pituitary is influenced by the level of sodium ion rather than the osmotic pressure.

Animals↗
PubMed1983

Norepinephrine induces releases of both LH-RH from the hypothalamus and LH from the rat pituitary in vitro.

The effects of norepinephrine (NE) on the release of luteinizing hormone (LH) and LH-releasing hormone (LH-RH) were examined in a sequential double chamber perifusion system by perfusing the medio-basal hypothalamus (MBH) and/or pituitaries excised from normal female rats in diestrus. When the pituitary alone or in sequence with the MBH was perifused with medium containing 200 micrograms/ml of NE, the concentration of LH in the efflux was significantly (p less than 0.05) increased to the level 50-150% over the pre-injection control, whereas medium without NE had no effect. Perifusion of the pituitary in sequence with the MBH produced a higher peak level of LH than that attained by the perifusion of the pituitary alone. Administration of NE induced a significant increase in LH-RH release from the MBH, although the medium alone had no effect. These data suggest that NE induces LH release from the pituitary both by increasing LH-RH release from the MBH and by its direct action on the pituitary.

Animals↗
PubMed1983

Clomiphene citrate induces luteinizing hormone release through hypothalamic luteinizing hormone-releasing hormone in vitro.

The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 X 10(-10) M oestradiol (E2), two significant peaks in LH release (60-130% increase, P less than 0.05) were observed 40 min and 90 min after the administration of 3 X 10(-8) mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25-50% increase, P less than 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50-100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.

Animals↗
PubMed1983

Arginine vasopressin suppresses oxytocin release from the superfused rat hypothalamo-pituitary complex.

The role of arginine vasopressin (AVP) in the regulation of oxytocin secretion was studied in a superfusion system of the hypothalamo-pituitary complex from cycling female rats in dioestrus of the oestrous cycle. After perfusion with Medium 199 alone at 37 degrees C for an equilibration period of 2.5 h, perfusion with Medium 199 containing 10 mU/ml AVP for 30 min caused a prompt and significant (P less than 0.05) decrease in the oxytocin level of up to 60% of that before AVP perfusion, whereas Medium 199 containing 0.1 mU/ml AVP had no effect on oxytocin efflux. This finding suggests that AVP may be involved in the regulation of oxytocin release from the hypothalamo-pituitary system.

Animals↗
PubMed1983

Prostaglandin D2 stimulates secretion of luteinizing hormone from pituitary gland in vitro.

The effect of prostaglandin D2 on the release of luteinizing hormone was studied in a superfusion system by superfusing human pituitary gland. Perfusion with 30 micrograms of prostaglandin D2 induced a significant increase of luteinizing hormone secretion. This is the first evidence of a direct effect of prostaglandin D2 on the secretion of luteinizing hormone from the human pituitary gland. This finding suggests the possible role of prostaglandin D2 in human reproductive function.

Adult↗
PubMed1983

Prostaglandin D2 induces release of luteinizing hormone from the rat pituitary gland without the modulation of hypothalamic luteinizing hormone releasing hormone.

The effect of prostaglandin D2 (PGD2) on release of LH and LH releasing hormone (LHRH) was studied in a sequential double-chamber superfusion system using the medial basal hypothalamus (MBH) and the pituitary gland from female rats at dioestrus. Infusion of PGD2 (5.7 or 57 mumol/l) caused a significant (P less than 0.05) increase in LH release to values 40-60% above the preinjection values from the pituitary gland superfused either alone or in series with the MBH. No release of LHRH in response to PGD2 was observed from the superfused MBH. These data demonstrate that PGD2 causes LH release from the pituitary gland not by inducing release of hypothalamic LHRH but by a direct action on the gland.

Animals↗
PubMed1982

Increase of fidelity of polypeptide synthesis by spermidine in eukaryotic cell-free systems.

The mechanism of spermidine-induced increase of fidelity of polypeptide synthesis in a wheat germ cell-free system has been studied. It was found that the increase of fidelity in the presence of spermidine occurred mainly at the level of binding of aminoacyl-tRNA to ribosomes, that reduction of misreading was more marked at the 5'-base than at the 3'-base of the codon and that misreading caused by paromomycin and kanamycin C was not significantly decreased by spermidine. It was deduced from these results that spermidine inhibited low-frequency misreading more strongly than high-frequency misreading. In addition, spermidine was found to stimulate the rejection of non-cognate aminoacyl-tRNA mainly at an initial discrimination step during the binding of amino-acyl-tRNA to ribosomes, and slightly at a subsequent GTP-dependent discrimination step, the so-called proofreading step. In yeast, rabbit reticulocyte, and Artemia salina cell-free systems, spermidine was found to increase the fidelity of protein synthesis.

Animals↗
PubMed1982

Radioimmunoassay for an analog of thyrotrophin-releasing hormone, gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide (DN-1417).

A heterologous radioimmunoassay method was established to determine plasma levels of gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide (DN-1417). As this compound is unstable in the incubation buffer, we introduced a conversion step. DN-1417 in the plasma was extracted with a solution of isopropanol-isobutylamine (4 : 1) and incubation was performed at room temperature for 2 h for the conversion of DN-1417 into N-[2-hydroxy-4-(isobutylcarbamoyl)butyryl]-L-histidyl-L-prolinamide (DN-isobutylamide). 125I-labeled 2-hydroxy-4-carboxybutyryl-L-histidyl-L-prolinamide and antisera, which was raised in the rabbit using an esterified derivative of DN-1417 conjugated with BSA as an antigen, were used for a sensitive radioimmunoassay of DN-isobutylamide. In this system, 0.2 ng DN-isobutylamide/ml plasma, equivalent to 0.16 ng DN-1417/ml, was detected and there was no apparent interference from its metabolites. The within-assay coefficients of variation were 7.6% at 7.73 ng/tube and 13.7% at 1.32 ng/tube. The between-assay coefficients of variation were 16.1% at 6.43 ng/tube and 12.2% at 1.20 ng/tube. The mean recovery rate of the assay system was 76.0 +/- 3.2% (S.E.M.).

Animals↗
PubMed1982

Restoration of oestrogen-positive feedback effect on LH release in women with prolactinoma by transsphenoidal surgery.

The effects of hyperprolactinaemia on the hypothalamo-pituitary axis by iv injection of 100 micrograms luteinizing hormone releasing hormone (LRH) in 7 women with prolactinoma before and 3 months after normalization of the Prl level by transsphenoidal surgery. A dose of 20 mg of conjugated oestrogen (Premarin) was also infected iv into patients with prolactinoma before and 4 months after surgery, and the serum LH levels were determined serially for 120 h after the injection. Surgical treatment caused significant reduction of the mean (+/- SE) serum prolactin (Prl) level from 123.3 +/- 7.8 to 19.4 +/- 5.6 ng/ml. But the differences in the basal levels of HL (11.3 +/- 2.2 to 8.6 +/- 1.5 mIU/ml), FSH (8.3 +/- 2.4 to 10.6 +/- 3.7 mIU/ml) and oestradiol (26.6 +/- 8.6 to 37.5 +/- 5.5 pg/ml) before and 4 months after surgery were not significant. An exaggerated LH response to LRH in untreated prolactinoma patients was also observed after surgical treatment. After surgical treatment, patients showed LH release with a peak between 48 and 72 h after the injection of Premarin, whereas before treatment they did not show any LH discharge. The mean percent increase in LH between 48 and 72 h was also significantly higher after operation than before operation. These results suggest that the hyperprolactinaemia in prolactinoma patients may cause an impaired positive feedback effect of oestrogen on LH release and that this derangement can be reversed by reduction of the Prl level by adenomectomy.

Adenoma, Chromophobe↗
PubMed1982

Progesterone facilitates the LRH releasing action of oestrogen.

The effects of progesterone (P) on the release of LRH and LH were examined in a sequential double chamber superfusion system by superfusing the medial basal hypothalamus (MBH) and/or pituitaries excised randomly from cycling female rats. Addition of 10 microliters of 10(-6) M oestradiol (E2) to the first chamber resulted in a gradual and significant (60-160%) increase in LH release above the pre-injection level from the pituitary in series with MBH. Administration of 10(-8) M P after 10(-6) M E2 caused a prompt and marked increase (300%) of LH (P less than 0.05), whereas 10(-8) M P alone had no effect. Administration of 10(-6) M E2, 10(-8) M P or E2 plus P did not significantly change LH secretion from the pituitary superfused alone. The concentration of LRH in the efflux was significantly increased (150-200%) 150 min after 10(-6) M E2 administration. P administration after E2 injection produced a prompt and significant increase of LRH and the increase of LRH (300-600%) was 2-3-fold that produced by E2. P alone had no effect. These data clearly indicate that P enhances E2-induced LH release by increasing LRH secretion from the MBH.

Animals↗
PubMed1982

Changes in luteinizing hormone-releasing hormone in human placenta throughout pregnancy.

The distribution and content of luteinizing hormone-releasing hormone (LH-RH) in human placental tissues were detected by enzymatic antibody and immunofluorescence techniques. Anti-LH-RH was taken up strongly by cytotrophoblasts and the villous stroma at 8 weeks of pregnancy; the uptake decreased with the progress of pregnancy. Anti-LH-RH was not taken up at all by syncytiotrophoblasts throughout pregnancy. These findings suggest that LH-RH is synthesized in the cytotrophoblast and villous stroma. The role of placental LH-RH in the synthesis of human chorionic gonadotropin is discussed.

Female↗