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Biomedical subjects

A Shimatsu

Publications and source records attributed to A Shimatsu.

At least 73 records · Page 4Linked to original sources
PubMed1991

Serotoninergic denervation suppresses the sympathetic outflow induced by thyrotropin-releasing hormone in conscious rats.

Intrathecal administration of thyrotropin-releasing hormone (TRH) resulted in an increase in plasma epinephrine (E) and glucose levels in conscious rats. To elucidate the mechanisms by which TRH stimulates the release of E, the animals were pretreated with 5,7-dihydroxytryptamine, parachlorophenylalanine, methysergide or ketanserin. Serotoninergic denervation suppressed the TRH-induced increase in plasma E and glucose levels, whereas inhibition of serotonin (5-HT) synthesis or blockade of 5-HT receptors did not suppress the responses. These findings suggest that the serotoninergic neurons, but not 5-HT itself, are involved in stimulating the sympathetic outflow by TRH at the spinal level.

5,7-Dihydroxytryptamine↗
PubMed1991

Cholinergic modulation of growth hormone secretion induced by galanin in rats.

The effects of cholinergic modulation by hexamethonium (HEX), tetraethylammonium (TEA), pirenzepine (PIR) and neostigmine on growth hormone (GH) secretion induced by galanin (GAL) were investigated in awake, freely moving male rats. Intracerebroventricular (i.c.v.) injection of GAL (0.6 nmol) caused a marked increase in plasma GH levels. Pretreatment with HEX (3 or 15 mg/kg BW), TEA (15 mg/kg BW) or PIR (0.5 mg/kg BW) significantly reduced the GAL-induced GH secretion. Pretreatment of animals with neostigmine (0.05 mg/kg BW) or with a specific antisomatostatin antiserum (10 microliters of 1:10 diluted with saline, i.c.v.) reversed the inhibition of GAL-induced GH secretion by HEX. These findings suggest that both nicotinic and muscarinic cholinergic mechanisms interact with the galanin-induced GH secretion by modulating hypothalamic somatostatin release.

Animals↗
PubMed1990

[Clinical application of a sensitive immunoradiometric assay for human growth hormone].

A sensitive immunoradiometric assay (IRMA) for human growth hormone (GH) using monoclonal antibodies was evaluated for clinical application. The detection limit of GH in serum was 0.05 ng/ml using 0.1 ml of serum. The specificity and assay precision were satisfactory. GH levels in serum determined by the IRMA were well correlated to those determined by the sensitive enzyme immunoassay or the commercial radioimmunoassay. Most of the basal GH levels in serum from normal adult subjects were detectable; mean values in male and female were 0.21 and 0.65 ng/ml, respectively. Serum GH levels decreased to less than 1 (0.5) ng/ml after oral glucose loading in normal subjects. Postoperative acromegalic patients were classified into two groups according to their GH responses to glucose. In group 1, GH levels were suppressed less than 1 ng/ml, suggesting normal GH dynamics. On the other hand, in group 2, GH levels remained elevated above 1 ng/ml, and postinhibitory rebound rise in serum GH after dopamine infusion was observed, suggesting the presence of residual adenoma tissues. Determination by sensitive IRMA of GH responses during oral glucose loading is useful for evaluating the activity of postoperative acromegaly.

Acromegaly↗
PubMed1990

Immunoreactive growth hormone (GH) secretion by human lymphocytes: augmented release by exogenous GH.

Peripheral blood mononuclear cells (PBMCs) from normal adults secreted small amounts of human growth hormone (GH; 0.2-0.6 pg/10(5) cells/7 days culture) as measured by a highly sensitive enzyme immunoassay. Stimulation of PBMCs with phytohemagglutinin (PHA) consistently showed a 4-6 fold increase in GH secretion. Transformed B-lymphocytes by Epstein-Barr virus also secreted GH (0.8-4.8 pg/5 x 10(4) cells/7 days culture). GH secreted by lymphocytes comigrated with pituitary GH on an Ultrogel AcA44 column. Addition of GH during the culture augmented endogenous GH secretion from PHA-stimulated PBMCs. GH-releasing hormone and a somatostatin analogue, SMS 201-995, did not affect GH secretion from non-stimulated and PHA-stimulated PBMCs. These findings suggest that both T and B lymphocytes secrete immunoreactive GH in a different manner from that in the anterior pituitary.

Adult↗
PubMed1990

Effects of intrathecal administration of thyrotropin releasing hormone and its analogue, DN1417, on plasma glucose and catecholamine levels in conscious rats.

Effects of intrathecal (i.t.) administration of TRH and the TRH analogue, DN1417, on plasma catecholamines and glucose levels were studied in conscious male rats. The i.t. administration of TRH (0.6 and 3 nmol) at the T8-10 vertebral level resulted in a dose-related increase in epinephrine (E), norepinephrine (NE), and glucose levels, which was suppressed by prior administration of the ganglionic blocker, hexamethonium (1.5 mg/100 g b. wt.). I.t. administration of TRH (3 nmol) caused small increases in plasma E and glucose at the C7-T1 vertebral level, but it did not change plasma E, NE and glucose levels at the sacral level. DN1417 (3 nmol) administered i.t. at the T8-10 or C7-T1 vertebral level had a more potent and long-lasting effect in stimulating the release of E than TRH. These findings suggest that TRH may act on sympathetic preganglionic neurons at the T7-10 spinal levels and stimulate the release of catecholamines from the adrenal medulla.

Animals↗
PubMed1990

Galanin-induced prolactin release in rats: pharmacological evidence for the involvement of alpha-adrenergic and opioidergic mechanisms.

The mechanism by which galanin (GAL) stimulates prolactin (PRL) secretion was investigated in urethane-anesthetized male rats. The PRL release induced by intracerebroventricular (i.c.v.) injection of porcine GAL (pGAL) was similar to that induced by rat GAL. The PRL release induced by pGAL was partially blocked by alpha-adrenergic antagonists, phentolamine (1 microgram/rat, i.c.v.; 29.1 +/- 4.5 ng/ml vs control 66.9 +/- 10.2 ng/ml, P less than 0.01) and tolazoline (1 microgram/rat, i.c.v.; 25.9 +/- 4.4 ng/ml vs control 59.6 +/- 10.9 ng/ml, P less than 0.05). Neither propranolol (1 microgram/rat, i.c.v.), a beta-adrenergic antagonist, nor prazosin (1 microgram/rat, i.c.v.), an alpha 1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 micrograms/100 g body wt., i.v. 30 min before), an opiate antagonist, also inhibited pGAL-induced PRL release (25.9 +/- 4.0 ng/ml vs 59.1 +/- 7.2 ng/ml, P less than 0.01). Combined treatment with naloxone and phentolamine caused greater inhibition of pGAL-induced PRL release than did phentolamine alone (10.3 +/- 1.5 ng/ml vs 23.2 +/- 4.7 ng/ml, P less than 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that alpha 2-adrenergic and opioidergic mechanisms are involved in PRL release induced by GAL.

Adrenergic alpha-Antagonists↗
PubMed1990

Barrel rotation in rats induced by SMS 201-995: suppression by ceruletide.

Intracerebroventricular administration of SMS 201-995 (5 micrograms/rat), a somatostatin analogue, induced barrel rotation in rats. Pretreatment with ceruletide (40 micrograms/100 g b. wt., IP) 3 days or 7 days prior to the injection of SMS 201-995 significantly inhibited the response rate of barrel rotation induced by SMS 201-995, but not that induced by arginine-vasopressin (1 microgram/rat, ICV). The suppressive effect of ceruletide on barrel rotation could be partially countered by MK-329, a selective peripheral CCK (CCK-A) receptor antagonist. Desulfated cerulein did not affect the barrel rotation induced by SMS 201-995. These findings suggest that ceruletide specifically suppresses the barrel rotation evoked by SMS 201-995 in a long-lasting manner possibly acting through CCK-A receptor.

Amino Acid Sequence↗
PubMed1990

Growth hormone and growth hormone binding protein in human urine.

The presence of growth hormone binding protein (GH-BP) in urine was demonstrated in normal subjects. Scatchard analysis showed that an association constant (Ka) and a maximum binding capacity (Bmax) of urinary GH-BP were 2.3 +/- 0.8 x 10(8) M-1 and 19.2 +/- 4.0 ng/mg urinary protein, respectively. The molecular weight of the urinary GH-BP was estimated to be 50000 to 70000 on gel chromatography. Although the molecular weight and Ka were similar to those of plasma GH-BP, Bmax of urinary GH-BP was significantly higher than that of plasma GH-BP (0.44 +/- 0.12 ng/mg protein). GH-BP in urine may be derived from plasma and/or renal tubules.

Adult↗
PubMed1990

Growth hormone responses to oral glucose loading measured by highly sensitive enzyme immunoassay in normal subjects and patients with glucose intolerance and acromegaly.

Plasma GH levels were determined during a 75-g oral glucose tolerance test using a highly sensitive enzyme immunoassay. Most normal subjects and patients with varying degrees of impaired glucose tolerance showed a decrease in plasma GH levels during the first 60 min. A GH rise within 60 min was observed in 3 of 37 normal subjects. The incidence of the GH rise (8%) was significantly lower than that (40%) in control experiments after water loading. The median minimum GH levels were 0.15 and 0.14 micrograms/L after glucose and water loading, respectively. Plasma GH responses to glucose ingestion were not different between normal subjects and patients with glucose intolerance. After surgery, 12 of 16 patients with acromegaly showed low basal GH levels (less than 5.0 micrograms/L). Six of the 12 patients showed normal GH responses to glucose loading (median minimum GH level, 0.21 micrograms/L) and normal plasma insulin-like growth factor-I levels. Plasma GH levels were not suppressed below 1.0 micrograms/L in the remaining 6 acromegalic patients. Determination of plasma GH levels after glucose loading by the highly sensitive enzyme immunoassay is useful for evaluating the effect of surgical treatment of acromegaly.

Acromegaly↗
PubMed1990

Secretory dynamics of growth hormone in an acromegalic patient associated with Graves' disease.

The dynamics of GH secretion were investigated in an acromegalic patient with Graves' disease during treatment with antithyroid drugs and radioactive iodine. The mean (+/- SE) basal plasma GH levels were 16.5 +/- 0.9 and 7.8 +/- 0.7 micrograms/L during the hyperthyroid and euthyroid states, respectively. There was a positive correlation (r = 0.902) between basal GH and free T4 levels. Twenty-four-hour plasma GH and urinary GH excretion both increased during the thyrotoxic state. Intravenous administration of TRH induced a marked increase in plasma GH levels during euthyroidism and a modest increase when the patient was hyperthyroid, whereas GH release induced by GH-releasing hormone was not altered by thyroid status. These findings suggest that hyperthyroidism stimulated spontaneous GH secretion from the pituitary adenoma, but inhibited the stimulating effect of TRH.

Acromegaly↗
PubMed1990

Evaluation of activity in postoperative acromegalics--plasma growth hormone levels during oral glucose tolerance test, daytime blood sampling and urinary GH excretion.

Plasma growth hormone (GH) levels during oral glucose tolerance test (OGTT) and during the daytime (0900-1700 h) and urinary GH excretion were determined in 6 normal subjects and 10 patients with postoperative acromegaly by means of a highly sensitive enzyme immunoassay (EIA). Acromegalic patients were divided into two groups according to their GH responses during OGTT. In group I patients plasma GH was suppressed below 1.0 microgram/l as in normal subjects, whereas GH levels persisted above 1.0 microgram/l in group II patients. Plasma GH profiles during the daytime were characterized by low nadir GH levels in normal subjects (0.21 +/- 0.10 microgram/l and group I patients (0.38 +/- 0.10 microgram/l) when compared with those in group II patients (4.7 +/- 2.0 microgram/l). Nadir GH levels during the daytime coincided with those during OGTT. Urinary GH excretions in group I patients (median 12 ng/day, range 4.3-29 ng/day) were within normal limits (2.6-20 ng/day) and significantly lower than those in group II patients (median 40 ng/day, range 19-130 ng/day.) Determination of plasma GH levels during OGTT and urinary GH excretion by the highly sensitive enzyme immunoassay is useful in evaluating the activity of postoperative acromegaly.

Acromegaly↗
PubMed1990

Secretion of alpha and TSH-beta subunits in patients with acromegaly: an in vivo study.

Plasma alpha and TSH-beta subunit responses to iv administration of GHRH were examined in 19 patients with active acromegaly. In 4 patients (21%), plasma alpha subunit levels were increased over 50% of basal levels after administration of GHRH, whereas plasma TSH-beta subunit levels were increased in response to GHRH in another 5 patients (26%). No patient showed simultaneous increases of alpha and beta subunits. After successful surgery, alpha and TSH-beta subunits did not respond to GHRH. These findings support the idea that some pituitary adenomas in acromegaly cosecrete GH and either alpha subunit or TSH-beta subunit.

Acromegaly↗
PubMed1989

[A multicenter clinical trial of SMS 201-995 (octreotide acetate) in acromegaly and gigantism].

Sixty-four patients with active acromegaly and three patients with gigantism were treated with the long acting somatostatin analog SMS 201-995 (50-500 micrograms, sc, every 6-12 h or 150-880 micrograms daily by intermittent sc infusion, for up to 114 weeks). The fasting plasma GH levels were significantly suppressed (less than 50% of the values before treatment) in 49 patients and became normal in 18 patients. Suppression of GH secretion was associated with normalization of plasma somatomedin-C levels (14 out of 30 cases) and significant clinical improvement such as disappearance of headache and decrease of excessive sweating. Shrinkage of pituitary tumors as determined by computed tomography and/or magnetic resonance imaging studies occurred in 11 out of 40 cases. Side effects were minimal and tolerable. SMS 201-995 appears to be an effective agent for the treatment of acromegaly and gigantism.

Acromegaly↗
PubMed1989

Effects of clonidine and naloxone on the dopamine levels in the rat mediobasal hypothalamus measured by in vivo voltammetry.

We examined the effect of alpha 2-adrenergic stimulation on dopamine (DA) levels in the mediobasal hypothalamus (MBH) by means of in vivo voltammetry in the rat. Intravenous (i.v.) injection of an alpha 2-agonist, clonidine (15 micrograms/100 g b.wt.) caused a decrease of MBH DA levels (76 +/- 3% of basal levels). Pretreatment with phenoxybenzamine (500 micrograms/100 g b.wt.i.v.), an alpha-antagonist, blunted the decrease of MBH DA levels induced by clonidine. Naloxone (125 micrograms/100 g b.wt.i.v.), an opioid antagonist, blunted the decrease of MBH DA levels induced by clonidine. These results suggest that alpha 2-adrenergic mechanisms may inhibit the tuberoinfundibular dopaminergic (TIDA) system through the activation of the endogenous opioid system.

Animals↗
PubMed1989

Possible mechanisms involved in growth hormone secretion induced by galanin in the rat.

The mechanisms by which central or systemic administration of galanin stimulates GH secretion were investigated in either conscious or urethane-anesthetized male rats. Intracerebroventricular injection of synthetic porcine galanin, a 29-amino acid gut-brain peptide (0.12, 0.6, and 3 nmol/rat), resulted in a dose-related increase in plasma GH. The plasma GH level was increased by an N-terminal galanin fragment [galanin-(1-19)], but not by C-terminal fragments [galanin-(2-29) and -(21-29)]. Intravenous injection or infusion of galanin (0.6 and 3 nmol/100 g BW) also raised plasma GH. The plasma GH increase induced by galanin was inhibited by pretreatment with rabbit antiserum specific for rat GRF. Pretreatment with yohimbine or phenoxybenzamine, alpha-adrenergic blockers, or picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, blunted the plasma GH increase induced by intracerebroventricular injection of galanin. On the other hand, the plasma GH increase induced by iv injection of galanin was suppressed by picrotoxin, but not by phenoxybenzamine. These findings suggest that 1) both central and systemic administration of galanin stimulate GH secretion in the rat; 2) the N-terminal structure of galanin is required to stimulate GH secretion; 3) the stimulating effect of galanin is mediated, at least in part, by hypothalamic GRF; and 4) central alpha-adrenergic and GABAergic mechanisms may be involved in GH release induced by central administration of galanin, whereas systemic injection of galanin stimulates GH release predominantly through GABAergic mechanisms in the rat.

Adrenergic alpha-Antagonists↗
PubMed1989

Urinary excretion of human growth hormone: daily variation and relationship with albumin and alpha 1-microglobulin in urine.

Urinary excretion of growth hormone during night-time was measured by a highly sensitive enzyme immunoassay in 6 normal men for 18-24 days. Urinary GH excretion distributed widely from 0.12 to 4.7 pg/mumol creatinine and the coefficient of variation in each subject ranged from 37 to 57% (mean 49%). Urinary excretion of albumin and alpha 1-microglobulin also showed moderate day-to-day variations (mean coefficients of variation: 37 and 42%, respectively). No correlation was found among urinary excretion of GH, albumin and alpha 1-microglobulin. Plasma and urinary GH levels were determined every 5 min and 2 h, respectively, from 09.00 h to 17.00 h in 4 normal men. Urinary GH excretion every 2 h during daytime closely reflected the change of plasma GH levels in each subject, suggesting that physiological GH secretory dynamics are reflected on the urinary GH excretion. Repeated measurements of urinary GH excretion are required to evaluate GH secretory capacity.

Adult↗
PubMed1989

Possible involvement of endogenous opioid peptides in prolactin secretion induced by alpha 2-adrenergic stimulation in rats.

Noradrenergic mechanisms have a stimulatory role in regulating prolactin (PRL) secretion in the rat. We investigated the mechanism by which the alpha 2-adrenergic system stimulates PRL release in urethane-anesthetized male rats. Intracerebroventricular injection of norepinephrine (2 micrograms/rat) or epinephrine (100 ng and 1 microgram/rat) caused an increase in plasma PRL levels. The PRL increase induced by epinephrine was much greater than that by norepinephrine. Intracerebroventricular injection of phentolamine (1 microgram/rat), an alpha-antagonist, blunted the plasma PRL increase induced by epinephrine (100 ng intracerebroventricularly). Plasma PRL levels were increased by intravenous injection of alpha 2-agonists, clonidine (15 micrograms/100 g of body wt), and xylazine (200 micrograms/100 g of body wt). Plasma PRL increase induced by clonidine or xylazine was suppressed by intravenous injection of naloxone (125 micrograms/100 g of body wt), an opiate antagonist. These findings suggest that alpha 2-adrenergic mechanisms stimulate pituitary PRL secretion, at least partly, by activating endogenous opioid peptides in the rat.

Animals↗