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Biomedical subjects

A Shimatsu

Publications and source records attributed to A Shimatsu.

At least 109 records · Page 6Linked to original sources
PubMed1983

Glucagon-induced somatostatin release from perifused rat hypothalamus: calcium dependency and effect of cysteamine treatment.

Somatostatin (SRIF) release from rat hypothalamus was investigated in vitro with a perifusion system. Glucagon (1 microM) and high potassium concentrations (56 mM) stimulated SRIF release in a calcium-dependent manner. Pretreatment of the rat with cysteamine (30 mg/100 g body weight, 7 h earlier) significantly reduced SRIF release from the hypothalamus in glucagon- and high potassium-stimulated states as well as in the basal state. SRIF release from rat hypothalamus was also stimulated by both dibutyryl cyclic AMP (1 mM) and theophylline (3 mM). These results suggest that glucagon, acting in a calcium-dependent manner and possibly through the adenylate cyclase-cyclic AMP system, stimulates SRIF release from rat hypothalamus and that cysteamine treatment reduces releasable SRIF in the hypothalamus.

Animals↗
PubMed1983

Effects of VIP, TRH, GABA and dopamine on prolactin release from superfused rat anterior pituitary cells.

Effects of VIP, TRH, dopamine and GABA on the secretion of prolactin (PRL) from rat pituitary cells were studied in vitro with a sensitive superfusion method. Dispersed anterior pituitary cells were placed on a Sephadex G-25 column and continuously eluted with KRBG buffer. Infusion of TRH (10(-11) - 10(-8)M) and VIP (10(-9) - 10(-6)M) resulted in a dose-related increase in PRL release. LHRH (10(-8) - 10(-5)M) had no effect on PRL release. On the other hand, infusion of dopamine (10(-9) - 10(-6)M) and GABA (10(-8) - 10(-4)M) suppressed not only the basal PRL release from dispersed pituitary cells but also the PRL response to TRH and VIP. The potency of TRH to stimulate PRL release is greater than that of VIP, and the potency of dopamine to inhibit PRL secretion is stronger than that of GABA on a molar basis. These results indicate that TRH and VIP have a stimulating role whereas dopamine and GABA have an inhibitory role in the regulation of PRL secretion at the pituitary level in the rat.

Animals↗
PubMed1983

Plasma calcitonin and ACTH responses to lysine vasopressin, calcium and pentagastrin in a patient with medullary thyroid carcinoma associated with Cushing's syndrome.

In a case study of medullary thyroid carcinoma (MTC) associated with Cushing's syndrome, elevated levels of urinary 17-hydroxycorticosteroids, plasma ACTH, cortisol, calcitonin (CT) and somatostatin (GHRIH) were documented. Lysine vasopressin administration further increased the levels of plasma ACTH, cortisol and CT, whereas the administration of calcium and pentagastrin increased only the level of plasma CT. Immunoreactive ACTH, CT and GHRIH were highly concentrated in the tumour tissues. Basal plasma ACTH levels were more progressively increased than plasma CT during the postoperative course when the patient was treated with o,p'-DDD, since the tumour was not completely resected. These findings suggest that the secretion of ACTH and CT from MTC were regulated in a different manner.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of prostaglandin E1 on vasoactive intestinal polypeptide release from the hypothalamus and on prolactin secretion from the pituitary in rats.

In order to elucidate the mechanisms by which prostaglandin (PG) affects PRL secretion, the effect of PGE1 on vasoactive intestinal polypeptide (VIP) release from the rat hypothalamus was examined by determining plasma VIP levels in rat hypophysial portal blood in vivo and VIP release from the perifused hypothalamus in vitro. Intraventricular injection of PGE1 (1 and 5 micrograms/rat) caused a 2- to 3-fold increase in the concentration of plasma VIP in hypophysial portal blood in anesthetized rats. The flow rate of portal blood was slightly increased after the injection of PGE1. VIP release from the perifused rat hypothalamus was stimulated by high potassium levels (56 mM). The infusion of PGE1 (10 microM) resulted in a significant increase in VIP release from the hypothalamus in vitro. Both these responses were calcium dependent. The intraventricular injection of PGE1 (1 and 5 micrograms/rat) resulted in a dose-related increase in peripheral plasma PRL levels in the rat. These findings suggest that PGE1 plays a stimulatory role in regulating VIP release from the hypothalamus into hypophysial portal blood and causes PRL secretion from the pituitary in rats.

Alprostadil↗
PubMed1983

Inhibition of prolactin secretion by gastrin releasing peptide (GRP) in the rat.

Synthetic gastrin releasing peptide (GRP) injected intraventricularly (1 microgram/rat), but not intravenously, suppressed rat prolactin (PRL) release induced by a Met-enkephalin analog, FK33-824 (10 micrograms/100 g body wt., iv). GRP also blunted PRL release induced by a dopamine antagonist, domperidone (1 microgram/100 g body wt., iv). In contrast, GRP did not suppress elevated plasma PRL levels sustained by a large dose of domperidone (10 micrograms/100 g body wt., iv). GRP (10(-5) M) had no effect on PRL release from superfused pituitary cells in vitro. These results suggest that GRP inhibits PRL secretion in the rat by acting through the brain to stimulate the dopaminergic mechanism.

Animals↗
PubMed1982

Effects of glucagon, Neurotensin, and vasoactive intestinal polypeptide on somatostatin release from perifused rat hypothalamus.

The effects of neuropeptides on the release of immunoreactive somatostatin (SRIF) from the rat hypothalamus were examined in vitro using a perifusion system. Twelve hypothalamic halves of male rats were placed on a Sephadex G-25 column and continuously eluted with Krebs-Ringer bicarbonate buffer, poH 7.4, at 37 C. A high potassium concentration (56 mM) stimulated SRIF release in a calcium-dependent manner. The infusion of glucagon (10(-7), 5 x 10(-7), and 10(-6) M) resulted in a dose-related increase in the release of SRIF. Neurotensin (10(-6) M) also stimulated SRIF release, whereas vasoactive intestinal polypeptide (10(-7) and 10(-6) M) inhibited SRIF release. SRIF release was not affected by cholecystokinin-octapeptide (10(-6) M), cholecystokinin-tetrapeptide (10(-6) M), or tRH (10(-6) M). These findings suggest that SRIF release from the rat hypothalamus is influenced by glucagon, neurotensin, and vasoactive intestinal polypeptide.

Animals↗
PubMed1982

Stimulation by serotonin of vasoactive intestinal polypeptide release into rat hypophysial portal blood.

The effect of serotonin (5-HT) on plasma vasoactive intestinal polypeptide (VIP) levels in hypophysial portal blood was studied in urethane-anesthetized rats. Portal blood was collected by the parapharyngeal approach and plasma VIP was determined by radioimmunoassay. Mean (+/- SE) basal plasma VIP level was 1799 +/- 232 pg/ml, which was slightly decreased during the control experiments in which physiological saline was injected either intraventricularly or intravenously. Intraventricular injection of 5-HT (2 and 10 micrograms/rat) resulted in a significant increase in plasma VIP concentrations within 20 min. Intravenous injection of L-5-hydroxytryptophan (5-HTP, 1 mg/100 g BW), a precursor of 5-HT, also caused an increase in VIP concentrations in hypophysial portal plasma. The flow rate of hypophysial portal blood did not change throughout the experiments. These findings suggest that 5-HT stimulates VIP release from the median eminence into the hypophysial portal vessels in the rat.

Animals↗
PubMed1982

Involvement of brain dopamine in prolactin secretion induced by a synthetic Met5-enkephalin analogue in rats.

The effect of a potent opioid peptide FK 33-824, [D-Ala2, MePhe4, Met(O)5-ol] enkephalin, on prolactin (PRL) release from rat anterior pituitary was investigated in vivo and in vitro. Systemic administration of FK 33-824 (1, 10 and 100 micrograms/100 g BW i.p.) caused a rapid and dose-related increase in plasma PRL in urethane-anesthetized male rats. Naloxone (125 micrograms/100 g BW i.v.) abolished PRL responses to FK 33-824. In the rat pretreated with either reserpine (2 mg/100 g BW i.p.), alpha-methyl-p-tyrosine (30 mg/100 g BW i.p.) or pimozide (50 micrograms/100 g BW i.v.), basal plasma PRL levels were elevated and FK 33-824 injection did not further increase plasma PRL. In contrast, neither 5,6-dihydroxy-tryptamine (50 micrograms/rat, i.c.v.) nor diphenhydramine (100 micrograms/100 g BW i.v.) treatment influenced the plasma PRL response to FK 33-824. FK 33-824 (10(-8)-5 X 10(-5) M) did not stimulate PRL release from dispersed anterior pituitary cells in vitro nor attenuate the inhibitory effect of dopamine (5 X 10(-7) M). These results suggest that central dopaminergic mechanisms are involved in PRL release induced by the opioid peptide.

Animals↗
PubMed1981

Involvement of alpha-adrenergic mechanisms in growth hormone release induced by opioid peptides in conscious rats.

The effects of synthetic enkephalin analog (KF 33-824) and beta-endorphin on growth hormone (GH) secretion and their interaction with brain monoamines were investigated in unanesthetized male rats. Blood samples (0.4 ml each) were withdrawn every 10-20 min for 6 h from a catheter chronically implanted in the right atrium. In all control rats, immunoreactive GH secretion was pulsatile in nature and two major GH bursts were found to occur around 12.00 and 15.30. The opioid peptides were injected between bursts at 14.00. Following an intravenous administration of FK 33-824 (10 microgram/100 g b.w.), there was an abrupt increase in plasma GH, which was significantly suppressed by naloxone (125 microgram/100 g b.w., i.v.), a specific opiate antagonist. Pretreatment with reserpine (1 mg/100 g b.w., i.p.) abolished not only the natural GH burst but also the GH response to FK 33-824. Pretreatment with dopamine-beta-hydroxylase inhibitors, diethyldithiocarbamate (DDC, 100 mg/100 g b.w., i.v.) and fusarate (10 mg/100 g b.w., i.v.) also inhibited the natural GH burst and GH rise induced by FK 33-824. Intravenous injection of clonidine (15 microgram/100 g b.w.), an alpha-adrenergic stimulant, resulted in an increase in plasma GH in the rats pretreated with reserpine, DDC or fusarate. Phenoxybenzamine (1 mg/100 g b.w., i.v.), an alpha-adrenergic blocking agent, inhibited the GH response to KF 33-824. On the other hand, GH release induced by FK 33-824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a beta-adrenergic blocking agent, nor pimozide (0.1 mg/100 g b.w., i.v.), a dopamine antagonist. Intraventricular administration of beta-endorphin (5 microgram/rat) also increased the plasma GH levels which were lowered by phenoxybenzamine. These findings suggest that alpha-adrenergic mechanisms are involved in GH release induced by opioid peptides in the rat.

Adrenergic alpha-Agonists↗
PubMed1981

Immunoreactive vasoactive intestinal polypeptide in rat hypophysial portal blood.

Vasoactive intestinal polypeptide (VIP) was measured by RIA in the hypophysial portal blood of rats after total hypophysectomy. The mean (+/- SE) VIP concentrations were 1332 +/- 171 pg/ml (range, 300-3868 pg/ml) under urethane anesthesia and 1735 +/- 707 pg/ml under pentobarbital anesthesia. The concentrations of VIP in peripheral plasma were, in most animals, less than 100 pg/ml. The secretion rate of VIP was not considerably changed during the blood collection. Immunoreactive VIP in hypophysial portal blood was identical to authentic VIP on gel chromatography. These findings suggest that VIP secreted from the hypothalamus may modulate pituitary function via the portal circulation. (Endocrinology 108: 395, 1981)

Anesthesia↗
PubMed1981

Possible involvement of gamma-aminobutyric acid in growth hormone release induced by a Met5-enkephalin analog in conscious rats.

The interaction between opioid peptides and gamma-aminobutyric acid (GABA) in regulating GH secretion was studied in unanesthetized male rats with chronically implanted intraatrial catheters. GH secretion was pulsatile with GH bursts (mean +/- SE, 259.1 +/- 70.3 ng/ml) occurring at regular intervals (mean +/- SE, 3.6 +/- 0.2 h) in control rats. When a potent met5-enkephalin analog, FK 33-824 ([D-Ala,MePhe4,Met(O)-ol]enkephalin; 10 micrograms/100 g BW), was injected iv in the interval between two anticipated spontaneous GH bursts, plasma GH abruptly increased to a peak value of 716.0 +/- 144.9 ng/ml 20 min after the injection, and the following spontaneous GH burst appeared at longer intervals than expected (5.0 +/- 0.4 h, P less than 0.025 vs. control). The plasma GH increase induced by FK 33-824 was blunted by a specific opiate antagonist, naloxone (125 micrograms/100 g BW, iv), and the following spontaneous GH bursts occurred at the same time as in controls. The plasma GH response to FK 33-824 was significantly inhibited by two GABA antagonists, picrotoxin (0.3 mg/100 g BW, iv) and bicuculline (60 micrograms/100 g BW, iv), with peak GH values of 24.6 +/- 6.4 and 136.4 +/- 35.2 ng/ml, respectively (P less than 0.01 vs. FK 33-824 alone). The following natural GH bursts were also inhibited by these GABA antagonists (50.1 +/- 21.3 and 35.3 +/- 9.6 ng/ml; P less than 0.01 vs. control). These findings suggest the possible involvement of GABA in GH release induced by opioid peptides in the rat.

Animals↗
PubMed1981

Stimulation of growth hormone release by vasoactive intestinal polypeptide from human pituitary adenomas in vitro.

The effects of vasoactive intestinal polypeptide (VIP), TRH, dopamine, and rat median eminence extract on GH release from GH-secreting pituitary adenomas were studied in vitro using a sensitive superfusion method. Dispersed pituitary tumor cells obtained from three patients with acromegaly were placed in a superfusion column, and the amounts of GH in the superfusate were determined. The addition of VIP (10(-6) M) to the perfusion system resulted in a marked increase in GH release in all three cases, and a dose-response relationship in VIP (10(-8) 10(-6) M) induced GH secretion was observed in one case studied. TRH (10(-7) M) and median eminence extract (1 equivalent/ml) also caused an abrupt and marked increase in GH release in all of the experiments. The infusion of either dopamine (10(-7) M) or bromocriptine (10(-7) M) inhibited GH secretion. These results suggest that VIP as well as TRH stimulate GH secretion by a direct action on GH-secreting pituitary tumor cells in at least some acromegalic patients.

Adenoma↗
PubMedDate not supplied

Involvement of hypothalamic somatostatin in glucagon-induced suppression of growth hormone secretion in conscious rats.

The role of central glucagon in regulating GH secretion was studied in conscious male rats with chronic indwelling intra-atrial and intracerebro-ventricular (ICV) cannulae. Repeated blood sampling every 20 min from 1000 hr to 1700 hr showed two major GH bursts occurring at regular intervals (3.6 +/- 0.1 hr) around 1200 hr and 1540 hr. The ICV (lateral ventricle) injection of glucagon (10 micrograms/rat) at 1100 hr inhibited spontaneous GH secretion, and the mean (+/- SE) plasma GH levels from 1120 hr to 1700 hr were lower than those in controls injected ICV with the vehicle solution only (31.9 +/- 7.8 ng/ml vs. 157.1 +/- 13.4 ng/ml, p less than 0.01). The GH bursts did not appear until 5 hr after the injection. The intravenous (IV) injection of glucagon (10 micrograms/rat) did not change plasma GH levels or the occurrence of spontaneous GH bursts. The glucagon-induced suppression of GH release was attenuated when anti-somatostatin serum (ASS), but not normal rabbit serum (NRS), was given IV in a volume of 0.25 ml immediately before the ICV injection of glucagon (10 micrograms/rat) (mean GH levels at 1120-1700 hr: ASS + glucagon, 133.6 +/- 26.7 ng/ml vs. NRS + glucagon, 30.5 +/- 7.4 ng/ml, p less than 0.01). These findings suggest that central glucagon may play an inhibitory role in regulating GH secretion by stimulating SRIF release from the hypothalamus in the rat.

Animals↗