Biomedical subjects

Y Osumi

Publications and source records attributed to Y Osumi.

At least 37 records · Page 2Linked to original sources

PubMed1995

Centrally applied bombesin increases nerve activity of both sympathetic and adrenal branch of the splanchnic nerves.

We reported that centrally applied bombesin probably excites both the gastric sympathetic and adrenomedullary systems and thus induces inhibition of gastric acid secretion. In the present study, therefore, we examined whether or not centrally applied bombesin directly affects sympathetic nerve activities in rats anesthetized with urethane. Intracerebroventricular administration of bombesin (0.3 and 3.0 nmol) increased discharge rates of the sympathetic branch as well as those of the adrenal branch of preganglionic greater splanchnic nerves. These effects were not secondary to changes in arterial blood pressure by bombesin. In conclusion, centrally applied bombesin directly activates both the sympathetic and adrenomedullary systems.

Action Potentials↗

PubMed1993

Microinjection of alpha-calcitonin gene-related peptide into the hypothalamus activates sympathetic outflow in rats.

Effect of rat alpha-calcitonin gene-related peptide (alpha-CGRP) microinjected into various hypothalamic nuclei on plasma levels of catecholamines and arterial blood pressure were investigated in urethane-anesthetized rats. alpha-CGRP (0.05 and 0.25 nmol) microinjected into the hypothalamic paraventricular nucleus (PVN) increased the plasma level of noradrenaline (NA), but not that of adrenaline (AD), in a dose-dependent manner. A similar increase in plasma level of NA was also observed by alpha-CGRP (0.05 nmol) microinjected into the preoptic area (POA), anterior hypothalamus (AH), dorsomedial hypothalamus (DMH) and ventromedial hypothalamus (VMH). A significant increase in arterial blood pressure was observed by microinjection of alpha-CGRP (0.05 nmol) into the PVN, POA, AH and DMH, and the most prominent increase was caused by its microinjection into the PVN. Microinjection of the same dose of this peptide into the VMH, lateral hypothalamic area and posterior hypothalamus was without effect. The increase in plasma level of NA induced by alpha-CGRP (0.05 nmol) into the PVN was not affected by bilateral adrenalectomy. Electrical stimulation of the PVN elicited increases in plasma levels of both NA and AD. This increase in NA was abolished by chemical sympathectomy with 6-hydroxydopamine (50 mg/kg, i.v., 3 days before experiments). These results suggest that activation of the PVN by electrical stimulation elicits both sympathetic and adrenomedullary outflow. alpha-CGRP microinjected into the PVN selectively activates the sympathetic outflow.

Adrenalectomy↗

PubMed1993

Central alpha 2-adrenoceptor-mediated inhibition of gastric motility in rats.

We investigated the subtype of alpha-adrenoceptors participating in central noradrenergic inhibition of gastric motility in urethane-anesthetized rats. Noradrenaline at 10 nmole administered intracisternally (i.c.) significantly decreased gastric motility. Yohimbine at 10 nmole, i.c., but not the same dose of prazosin, abolished this noradrenaline-induced decrease in gastric motility. Clonidine at 10 nmole, i.c., but not phenylephrine at 20 nmole, significantly decreased gastric motility. These results suggest that alpha 2-adrenoceptor-mediated mechanisms in the brain stem are involved in noradrenergic inhibitory regulation of gastric motility.

Adrenergic alpha-Agonists↗

PubMed1993

Ulcerative colitis in female siblings with an identical human leukocyte antigen haplotype (A24, Bw52, DR52 and DQw1).

Two female siblings with ulcerative colitis are reported. Both the 30-year-old elder sister and the 28-year-old younger sister developed bloody stools and diarrhea; ulcerative colitis was diagnosed by endoscopic and histologic examination of the colon. Their maternal aunt also suffered from the disease. Human leukocyte antigen analysis revealed an identical haplotype for the sisters (A24, Bw52, DR2 and DQw1), while the aunt had A24, Bw52 and DR2. The haplotypes of Japanese patients with familial ulcerative colitis are reviewed, and the role of human leukocyte antigens in this disease is discussed.

Adult↗

PubMed1993

Release of endogenous acetylcholine from a vascularly perfused rat stomach in vitro; inhibition by M3 muscarinic autoreceptors and alpha-2 adrenoceptors.

We measured endogenous overflow of acetylcholine (ACh) from a vascularly perfused rat stomach in vitro with modified Krebs-Ringer solution containing 100 microM physostigmine. Evoked ACh overflow by vagal stimulation at 2.5 Hz for 2 min was abolished by tetrodotoxin (3 x 10(-7) M) or Ca++ removal and reduced by hexamethonium (10(-4) M). The evoked overflow was inhibited by oxotremorine (10(-7) to 10(-5) M), but not attenuated by 4-(N-[3-chlorophenyl]carbamoyloxy)-2-butynyltrimethylammonium chloride (10(-6) and 10(-5) M). The evoked ACh overflow was enhanced by atropine (10(-9) to 10(-6) M), 4-diphenylacetoxy-N-methylpiperidine (10(-8) to 10(-6) M), methoctramine (10(-8) to 10(-6) M) and pirenzepine (10(-8) to 10(-6) M) in a concentration-dependent manner with the following potency; atropine > 4-diphenylacetoxy-N-methylpiperidine > methoctramine > pirenzepine. In the presence of 10(-6) M atropine, clonidine (10(-8) and 10(-7) M), but not phenylephrine (10(-7) and 10(-6) M), concentration-dependently decreased the evoked overflow of ACh at 1 Hz. Electrical stimulation of periarterial gastric sympathetic nerves (5 and 10 Hz for 2 min) frequency-dependently inhibited the evoked ACh overflow at 1 Hz in the presence of atropine and sympathetic inhibition mediated at 5 Hz was abolished by 10(-6) M rauwolscine, but not by 10(-6) M prazosin. These results indicate that the ACh release from gastric parasympathetic neurons is inhibited by M3 muscarinic autoreceptors and alpha-2 adrenoceptors.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1993

Roles of central nicotinic receptors in regulation of gastric functions.

In the first part of this paper, the effects of single administration of nicotine on gastric motility of urethane-anesthetized rats are briefly summarized from our recently reported papers. Then, the effects of repeated administration of nicotine on the nicotine-induced changes in gastric motility and release of hypothalamic noradrenaline, in vitro, are described, with special references to up-regulation of nicotinic receptors. Nicotine 0.1 nmol administered into the dorsal motor nucleus of the vagus (DMV) elicited a dual change, a decrease followed by an increase in gastric motility. Intravenous administration of nicotine 300 nmol/kg decreased gastric motility. This decrease in gastric motility was inhibited by microinjection of hexamethonium into the DMV and was terminated by bilateral vagotomy. In animals pretreated with nicotine 200 nmol intracerebroventricularly (icv) administered once a day for 5 days, nicotine 100 nmol administered icv induced the decrease but not the increase in gastric motility. In conclusion, nicotine activates nicotinic receptors in the DMV and a resultant vagally-mediated dual change in gastric motility occurs. Furthermore, gastric inhibitory mechanisms in the DMV are susceptible to nicotine more than the excitatory mechanisms, and desensitization to nicotine occurs easily in the excitatory mechanisms.

Animals↗

PubMed1993

Cholinergic M2 muscarinic receptor-mediated inhibition of endogenous noradrenaline release from the isolated vascularly perfused rat stomach.

We measured endogenous noradrenaline (NA) overflow from a vascularly perfused rat stomach in vitro. The stomach was perfused with Krebs-Ringer solution containing 10 microM pargyline. Periarterial nerves, which contain postganglionic sympathetic nerves, around the left gastric artery were stimulated for 1 min with square-wave pulses of 2 msec duration, 2.5 to 5.0 Hz, supramaximal intensity (10 mA). Oxotremorine (10(-8) to 10(-6) M) concentration-dependently inhibited the periarterial nerve stimulation-evoked NA overflow under the presence of 10(-6) M phentolamine. Bilateral vagus nerve stimulation (5 Hz, 2 msec duration, 10 mA, for 1 min) reduced the evoked NA overflow. Oxotremorine (10(-7) M)-induced inhibition of NA overflow was attenuated by atropine, methoctramine (muscarinic M2 receptor antagonist), 4-diphenylacetoxy-N-methylpiperidine (M3 receptor antagonist) and pirenzepine (M1 receptor antagonist) with the following potency; atropine > methoctramine > 4-diphenylacetoxy-N-methylpiperidine >> pirenzepine. The oxotremorine-induced inhibition was attenuated by N-ethylmaleimide (3 x 10(-5) M for 50 min), but was not affected by pertussis toxin pretreatment (10 micrograms/rat, for 4 days). However, this pretreatment with pertussis toxin abolished completely negative chronotropic and inotropic effects of oxotremorine in rat atria. These results suggest that NA release from gastric sympathetic nerve terminals is inhibited by activation of muscarinic M2 receptor, and this receptor-mediated inhibitory mechanisms are insensitive to pertussis toxin.

Animals↗

PubMed1992

Central noradrenergic inhibition of gastric motility in rats.

The roles of central noradrenergic mechanisms in the regulation of gastric motility were investigated in urethane-anesthetized rats in whom an intragastric balloon had been placed. Noradrenaline 100 nmol administered intracerebroventricularly (i.c.v.) significantly decreased spontaneous contractions of the stomach and this decrease in gastric motility was not observed in bilaterally vagotomized animals. Intracisternally administered (i.c.) noradrenaline (10 nmol) induced a decrease in gastric motility comparable to that elicited by noradrenaline 100 nmol i.c.v. Phentolamine 10 nmol i.c. but not the same dose of propranolol i.c. significantly antagonized the noradrenaline (10 nmol)-induced inhibition of gastric motility. These results suggest that alpha-adrenoceptor-mediated noradrenergic mechanisms in the brain stem are involved in the inhibitory regulation of gastric motility.

Animals↗

PubMed1992

Release of endogenous noradrenaline from the vascularly perfused rat stomach in vitro: modulation by pre- and postsynaptic adrenoceptors.

We developed an experimental in vitro model to detect a very small amount of endogenous noradrenaline (NA) released from the rat gastric sympathetic nerve terminals. The stomach was perfused via celiac artery with modified Krebs-Ringer solution containing 10 mM pargyline and 0.1% bovine serum albumin at a constant flow of 4 ml/min. The right greater splanchnic (SPL) nerve (preganglionic nerve of the gastric sympathetic nerve) was stimulated electrically with square-wave pulses of 2 msec duration and supramaximal intensity (5 mA) for 1 min. The rat stomach contained about 750 ng of NA and spontaneous overflow was about 0.05% of tissue content per 2 min. The NA overflow induced by SPL nerve stimulation at 5 Hz was abolished by tetrodotoxin (3 x 10(-7) M) and by Ca(++)-free medium containing 2 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid. Hexamethonium (5 x 10(-4) M) significantly decreased the NA overflow induced by SPL nerve stimulation at 5 Hz. Yohimbine (10(-7) and 10(-6) M) and prazosin (10(-7) and 10(-6) M) dose-dependently enhanced the NA overflow induced by SPL nerve stimulation at 5 Hz. Clonidine (10(-7) and 10(-6) M) and methoxamine (10(-5) M) significantly decreased the NA overflow induced by SPL nerve stimulation at 1 Hz and this methoxamine-induced inhibition was abolished by 8-(p-sulfophenyl)-theophylline (5 x 10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Spinal cord substance P mediates the inhibition of gastric acid secretion induced by electrical stimulation of the preoptic area.

A possible role of spinal substance P (SP) in the mediation of signals to inhibit gastric acid secretion by central activation of the sympatho-adrenomedullary system was examined in urethane-anesthetized rats. Intrathecal (i.t.) administration of SP (1-10 nmol) inhibited vagally induced acid output. I.t. administration of spantide, a SP receptor antagonist, reduced the inhibitory effect of 3 nmol SP. I.t. administration of spantide (0.1-1 nmol) blocked the inhibition of vagally induced gastric acid output evoked by electrical stimulation of the preoptic area. Atropine, hexamethonium, phentolamine, propranolol, DL-para-chlorophenylalanine (PCPA) and 5,7-dihydroxytryptamine (5,7-DHT) were without effect. Repeated i.t. administration of 10 nmol SP produced desensitization to the SP-induced inhibitory response on gastric acid output. In these animals, electrical stimulation of the preoptic area did not inhibit vagally induced gastric acid output. These results suggest that electrical stimulation of the preoptic area excites SP-containing neurons in the spinal cord, and a resultant sympatho-adrenomedullary system-mediated inhibition of gastric acid secretion occurs.

Animals↗

PubMed1991

Chemical sympathectomy with 6-hydroxydopamine potentiates intracerebroventricularly applied bombesin-induced increase in plasma adrenaline.

Intracerebroventricular administration of bombesin induced a marked increase in plasma level of adrenaline and a slight increase in that of noradrenaline in rats anesthetized with urethane. The bombesin-induced increase in adrenaline was potentiated by chemical sympathectomy with 6-hydroxydopamine (6-OHDA). On the other hand, adrenalectomy did not affect plasma level of noradrenaline in the bombesin-treated animals. In the splanchnicotomized rats, direct stimulation of the adrenal glands by intravenously administered nicotine increased plasma level of both adrenaline and noradrenaline. These increases were, however, not potentiated by chemical sympathectomy with 6-OHDA. Pretreatment with capsaicin, a potent toxin selective to sensory neurons, potentiated the bombesin-induced increase in plasma level of adrenaline. In these capsaicin pretreated rats, chemical sympathectomy did not potentiate the bombesin-induced increase in plasma level of adrenaline to any great extent. These results suggest that chemical sympathectomy with 6-OHDA potentiated the bombesin-induced increase in plasma adrenaline probably due to a disinhibitory activation of the splanchnic nerve by as yet unidentified but capsaicin sensitive neuron mechanisms.

Adrenalectomy↗

PubMed1991

Involvement of nicotinic receptors in the dorsal motor nucleus of the vagus in regulation of gastric motility in rats.

Roles of nicotinic receptors in the dorsal motor nucleus of the vagus (DMV) in the regulation of gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. Nicotine (0.1 nmole) microinjected into the DMV but not the nucleus ambiguus induced dual changes, a decrease followed by an increase in gastric motility. Administration of 0.1 nmole of hexamethonium into the DMV significantly inhibited the decrease in gastric motility induced by intravenously administered nicotine.

Animals↗

PubMed1990

CRT display visibility in automobiles.

Three experiments were carried out into aspects of CRT display in the context of driving automobiles. The first focused on the combination of colours which renders information 'easy-to-read', and determined the relationship between luminance contrast and chromaticity difference. In the second a background luminance which was not dazzling at night was expressed in a chromaticity diagram. In the third the amount of information which can be read 'at-a-glance' was investigated.

Automobiles↗

PubMed1990

Effects of prazosin HCl on the urethral pressure profile in patients with benign prostatic hyperplasia.

The effects of prazosin HCl on the urethral pressure profile (UPP) were studied in 14 patients with benign prostatic hyperplasia. Urethral pressure profilometry was performed 1 h after oral administration of 1 or 2 mg prazosin HCl. Functional profile and continence zone lengths were significantly reduced following administration of 1 or 2 mg prazosin HCl, as compared with the pretreatment lengths. The administration of 2 mg prazosin HCl resulted in a significant decrease in prostatic peak pressure, whereas the maximum urethral closure pressure exhibited an insignificant decrease. The results suggest that the effects of prazosin HCl on UPP were dose dependent within the range from 1 to 2 mg.

Aged↗

PubMed1990

[Central neurotransmitters and regulation of gastric acid secretion].

Central neurotransmitter and/or neuromodulator candidates reported to affect gastric acid secretion are: (excitatory) acetylcholine, thyrotropin releasing hormone, GABA, oxytocin; (inhibitory) noradrenaline, adenosine, bombesin, calcitonin-gene related peptide, corticotropin releasing factor, beta-endorphin, neurotensin, neuropeptide Y, insulin-like growth factor II and prostaglandins. Regulation of gastric acid secretion by central administration of these substances in experimental animals such as rats and dogs are briefly reviewed, and central inhibitory mechanisms of this function are discussed based on our studies with noradrenaline and bombesin. Roles of hypothalamic nuclei such as the ventromedial nucleus and the lateral hypothalamus in regulation of autonomic nerve activities are also described as an introductory note.

Animals↗

PubMed1990

Central inhibition of gastric motility by intravenously administered nicotine in rats.

Effects of intravenously (i.v.) administered nicotine on gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. I.v. administered nicotine at 75-300 nmole/kg dose-dependently decreased gastric motility. Decrease in gastric motility induced by nicotine at the dose of 300 nmole/kg was inhibited by intracisternally administered hexamethonium. Gastric motility was also decreased by intracisternally applied nicotine (1-10 nmole). These doses were much smaller than those by the intracerebroventricular route in our previous report. Bilateral vagotomy significantly suppressed basal gastric motility. In bilaterally vagotomized animals, nicotine at 1 mumole/kg but not 300 nmole/kg given i.v. significantly decreased the gastric motility maintained at a normal level by electrical stimulation of the vagus nerve. This nicotine-induced decrease in gastric motility, under conditions of electrical stimulation of the vagus nerve, was inhibited by pretreatment with phentolamine. These results suggest that a smaller dose of nicotine given i.v. activates nicotinic receptors in the brainstem and elicits vagally-mediated inhibition of gastric motility. Activation of peripheral alpha-adrenergic mechanisms together with that of central nicotinic mechanisms may be involved in the decreasing effects of a larger dose of nicotine on gastric motility.

Anesthesia↗

PubMed1989

Dual effect of nicotine injected in the cerebral ventricles on rat gastric motility.

Intracerebroventricularly (i.c.v.) administered nicotine 50 and 100 nmol produced dual changes, an early decrease and a successive increase in gastric motility in urethane-anesthetized rats in which an intragastric balloon had been placed. These dual effects of nicotine were significantly antagonized by simultaneously administered hexamethonium i.c.v. but not by splanchnicectomy or by pretreatment with reserpine. Both atropine pretreatment and vagotomy abolished the stimulating effect of nicotine on gastric motility. Nicotine administered i.c.v. to bilaterally vagotomized rats did not affect gastric motility which was however enhanced by electrical stimulation of the vagus nerve. These observations suggest that central activation of the vagal cholinergic component results in excitation and central activation of the vagal non-adrenergic inhibitory component with i.c.v. administered nicotine results in inhibition of gastric motility. Sympathoadrenal systems and central monoaminergic mechanisms are probably not involved in the inhibitory effect of i.c.v. administered nicotine on gastric motility.

Animals↗

PubMed1989

Central depletion of dopamine in rats by 1-methyl-4-phenylpyridine.

Effects of 1-methyl-4-phenylpyridine(MPP+), a putative neurotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP), on the contents of dopamine were examined in the various regions of the rat brain. Under anesthesia with pentobarbital sodium and flunitrazepam, MPP+ 150 micrograms/rat was intracerebroventricularly infused for 5 hours, at 30 micrograms/100 microliters/hr. Seven days later, the contents of dopamine, but not those of noradrenaline and activities of choline acetyl transferase in the brain were found to be significantly decreased, as compared to findings in the respective controls. The MPP+-induced depletion of dopamine was most evident in the striatum (38% of control). Contents of dopamine in the substantia nigra and ventral tegmental area were not significantly affected by MPP+. These results are interpreted to mean that intracerebroventricular continuous infusion of MPP+, in a relatively low concentration, induces a moderate but relatively specific disruption of central dopaminergic nerve terminals in rats, presumably by the selective accumulation of this neurotoxic agent into these nerve terminals.

1-Methyl-4-phenylpyridinium↗