Biomedical subjects

Y Osumi

Publications and source records attributed to Y Osumi.

At least 55 records · Page 3Linked to original sources

PubMed1989

Dual effects on gastric acid secretion of electrical stimulation of anterior parts of the rat hypothalamus.

The effect of electrical stimulation of anterior parts of the hypothalamus on gastric acid secretion was examined in rats anesthetized with urethane. Electrical stimulation (0.5 mA, 2 msec, 10 Hz, for 10 min) of the lateral hypothalamic area (LHA) induced a marked increase in basal gastric acid output. Electrical stimulation of the preoptic area (PO), the paraventricular nucleus (PVN) and the anterior hypothalamus (AH) also induced increases in basal acid secretion. Electrical stimulation of the PO, PVN and AH inhibited the increase in acid secretion induced by electrical stimulation of the vagus nerve (1 mA, 0.5 msec, 3 Hz). These inhibitory effects were abolished by bilateral cutting of the splanchnic nerves. On the other hand, the stimulation of the LHA had no effects on vagally stimulated gastric acid secretion. Electrical stimulation of the anterior parts of the hypothalamus induces dual effects, vagally mediated increases in basal gastric acid output and splanchnic mediated inhibition of the vagally stimulated gastric acid output.

Animals↗

PubMed1989

Dual effects of intracerebroventricularly applied nicotine on gastric motility in rats.

Intracerebroventricularly (i. c. v.) administered nicotine induced a decrease followed by an increase in gastric motility in urethane-anesthetized rats. These effects of i. c. v. administered nicotine were antagonized by simultaneously i. c. v. administered hexamethonium. Both vagotomy and pretreatment with atropine abolished the increasing effect of i. c. v. administered nicotine. In vagotomized rats, i. c. v. administered nicotine did not cause any decrease in gastric motility after elevation by electrical stimulation of the vagus nerve. These results suggest that i. c. v. administered nicotine activates central nicotinic receptors and that the vagus nerve is involved in both the inhibitory and stimulatory effects of i. c. v. administered nicotine on gastric motility.

Animals↗

PubMed1988

Alpha-2-adrenoceptor-mediated inhibition of vagally induced gastric acid secretion with the anti-ulcer agent DQ-2511.

Effects of DQ-2511, a new peripherally acting anti-ulcer agent, on vagally induced gastric acid output and mucosal blood flow (MBF) were investigated in urethane-anesthetized rats with gastric fistula. Intravenous infusion of DQ-2511 (2 or 20 mg/kg/hr, for 30 min) reduced the vagally induced gastric acid output and MBF, and these inhibitory effects were abolished by pretreatment with phentolamine. The DQ-2511-induced inhibition of acid output was abolished with yohimbine, but not with prazosin. These observations suggest that DQ-2511 possesses the properties of an adrenergic alpha-2-adrenoceptor agonist. DQ-2511 presumably acts on adrenergic alpha-2-adrenoceptors located on the parasympathetic neurons in the gastric wall, thereby reducing the vagally-induced gastric acid output.

Animals↗

PubMed1988

Sympathoadrenomedullary system mediation of the prostaglandin E2-induced central inhibition of gastric acid output in rats.

Mechanisms related to the gastric antisecretory action of i.c.v.-administered prostaglandins (PGs) were investigated in urethane-anesthetized rats with gastric fistula. The gastric acid output was enhanced by electrical stimulation of the left cervical vagus nerve after cutting the bilateral cervical vagus nerves. Intracerebroventricular administered PGE2 (0.05-0.5 microgram/animal) dose-dependently inhibited the vagally stimulated acid output whereas the same doses of PGE2 administered i.v. were without effect. The inhibitory effect of PGE2 (0.1 microgram/animal, i.c.v.) was more potent than the effects of the same doses of PGD2 and PGF2 alpha (PGE2 greater than PGD2 greater than PGF2 alpha). PGE2 (0.1 microgram/animal)-induced inhibition of the gastric acid output was abolished by splanchnicectomy, cutting the preganglionic splanchnic nerves under diaphragm, or by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg i.v., 3 days before). This PGE2-induced inhibition was also abolished by pretreatment with phentolamine (5 mg/kg i.m.), but not by propranolol (5 mg/kg i.m.). These observations suggest that the i.c.v.-administered PGs, in particular PGE2, induces a central excitation of the sympathoadrenomedullary outflow and that the resultant activation of gastric alpha adrenoceptors inhibits the vagally stimulated gastric acid output.

Adrenal Medulla↗

PubMed1987

Sympatho-adrenomedullary system mediation of the bombesin-induced central inhibition of gastric acid secretion.

Possible mechanisms of the inhibitory effect of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular (i.c.v.) administration of bombesin (0.1-3 nmol) dose dependently inhibited the increase in gastric acid secretion induced by both intravenous (i.v.) administration of 2-deoxy-D-glucose 60 mg/kg and electrical stimulation of the vagus nerve (1 mA, 0.5 ms, 3 Hz), but not increase due to i.v. infusion of bethanechol (10 micrograms/kg per min). Such an inhibitory effect of bombesin on the gastric response was markedly reduced by bilateral cutting of the greater splanchnic nerves. The inhibitory effect of bombesin on gastric acid secretion induced by stimulation of the vagus nerve was not modified either by chemical sympathectomy with 6-hydroxydopamine or by bilateral adrenalectomy alone. However, this inhibitory effect of bombesin was abolished under conditions of combined chemical sympathectomy and adrenalectomy. These results suggest that bombesin (i.c.v.) probably excites the sympatho-adrenomedullary system and thus induces inhibition of gastric acid secretion. Furthermore, a dysfunction of the sympathetic or of the adrenomedullary system may well be functionally compensated for by the system with unaltered function.

Adrenal Medulla↗

PubMed1987

Enhancement of gastric acid output and mucosal blood flow by tripeptide thyrotropin releasing hormone microinjected into the dorsal motor nucleus of the vagus in rats.

Central effect of thyrotropin releasing hormone (TRH) on gastric acid output and mucosal blood flow (MBF) was examined in urethane anesthetized rats. TRH, microinjected into the dorsal vagal complex [the dorsal motor nucleus of the vagus (NDV), the nucleus tractus solitarius and area postrema] induced dose-dependent (0.5-50 pmole) increases in gastric acid output and MBF. In contrast, 5 pmole TRH microinjected into various hypothalamic regions had no effect on these gastric parameters. Administration of TRH intraventricularly (i.c.v.) also increased these gastric parameters; however, about a 10 times higher dose of TRH was required to obtain the same order of excitatory effects seen with microinjection to the dorsal vagal complex. Application of anti-TRH serum to the dorsal vagal complex inhibited the increases in gastric acid output and MBF induced by TRH (i.c.v.). The effect of TRH applied to the dorsal vagal complex and i.c.v. were not modified by a concomitant administration of atropine. These results suggests that NDV is probably the site of action of TRH in inducing gastric hyper-functions. The mode of action of TRH seems to be independent of cholinergic muscarinic mechanisms present in the NDV.

Animals↗

PubMed1987

Effects of DJ-7141, a new peripherally acting alpha-2 adrenoceptor agonist, on blood pressure and gastric acid output in rats: evidence for the heterogeneity of alpha-2 adrenoceptors in different organs.

Effects of intravenously administered clonidine and DJ-7141 on blood pressure and gastric acid output were studied in anesthetized rats. Both drugs caused a dose-dependent increase in blood pressure. Clonidine-induced increases in the blood pressure were attenuated by yohimbine and prazosin. DJ-7141-induced increases in blood pressure were also attenuated by yohimbine, but were little affected even by a large dose of prazosin. Splanchnic nerve stimulation-induced increases in blood pressure were attenuated by clonidine and DJ-7141. The inhibitory effects of DJ-7141 exceeded those of clonidine. On the other hand, these agonists had no effect on exogenously applied norepinephrine-induced increases in blood pressure. Vagally stimulated gastric acid output was inhibited by small doses of clonidine and large doses of DJ-7141. Clonidine-induced inhibition of acid output was abolished by yohimbine (5 mg/kg), but not by prazosin (5 mg/kg). In contrast, the DJ-7141-induced inhibition of acid output was not affected by yohimbine (5 mg/kg), but was attenuated by a small dose of prazosin (0.1 mg/kg). These results indicate that DJ-7141 had no effect on alpha-2 adrenoceptors in gastric parasympathetic nerves. Furthermore, the alpha-2 adrenoceptors on parasympathetic nerves in the gastric wall are probably pharmacologically different from those on sympathetic nerves and blood vessels in rats.

Adrenergic alpha-Agonists↗

PubMed1987

Central site of inhibitory action of bombesin on gastric acid secretion in rats.

Sites of inhibitory action of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular administration of bombesin (3-1000 pmole) dose-dependently inhibited the increase in gastric acid secretion induced by electrical stimulation of the vagus nerve (1 mA, 0.5 msec, 3 Hz). On the other hand, intrathecal (direct lumbar puncture) administration of bombesin, even in the large dose of 1 nmole, had no effect on the vagally stimulated gastric acid secretion. Three pmoles of bombesin microinjected into the preoptic area, the anterior hypothalamus and the paraventricular nucleus inhibited the vagus stimulated gastric acid secretion. Microinjection of this peptide into the ventromedial nucleus, the dorsomedial nucleus and the lateral hypothalamic area were without effect. A large electrolytic lesion of the anterior hypothalamus, including the preoptic-anterior hypothalamic area and the paraventricular nucleus, abolished the inhibitory effect of intracerebroventricularly applied bombesin, but a lesion restricted to the preoptic-anterior hypothalamus or the paraventricular nucleus was without effect. We propose that the preoptic area, the anterior hypothalamus and the paraventricular nucleus are all involved in the inhibitory effect of bombesin on gastric acid secretion.

Animals↗

PubMed1987

Intracerebroventricularly administered nicotine inhibits vagally stimulated gastric acid output in rats by activating the central sympatho-adrenal outflow.

The effect of intracerebroventricularly (i.c.v.) administered nicotine was investigated in urethane-anesthetized rats. I.c.v., but not intravenously, administered nicotine (300 and 600 nmole/animal) inhibited the increase in gastric acid output induced by electrical stimulation of the vagus nerve. This antisecretory effect of nicotine was abolished by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg, i.v., 3 days before). I.c.v.-administered nicotine also raised the blood levels of catecholamines. These observations suggest that i.c.v. administered nicotine leads to excitation of the central sympatho-adrenomedullary outflow and inhibits gastric acid output induced by stimulation of the vagus nerve.

Adrenalectomy↗

PubMed1986

Sympatho-adrenal system involved in the inhibitory effects of nicotine on the vagally stimulated gastric acid output and mucosal blood flow in rats.

The peripheral effects of nicotine on gastric functions were examined in anesthetized rats. The intravenous infusion of nicotine inhibited the increase in vagally stimulated gastric acid output. This inhibitory effect was abolished by phentolamine or by a combined treatment with bilateral adrenalectomy and reserpine. Nicotine had a dual effect on the gastric mucosal blood flow (MBF): inhibition followed by an increase. The inhibitory effect was abolished by phentolamine or by the combination with reserpine and adrenalectomy. Propranolol or adrenalectomy abolished the increase. These various effects of nicotine on the gastric acid output and MBF were not attenuated by bilateral splanchnicectomy. These results suggest that nicotine acts directly on both the adrenal medulla and postganglionic sympathetic neurons in the gastric wall, namely by acting on alpha-adrenoceptors, thus decreasing acid output and MBF, and by activating beta-adrenoceptors thus slightly increasing MBF.

Adrenal Glands↗

PubMed1986

Nicotine applied into the dorsal motor nucleus of the vagus inhibits enhanced gastric acid output and mucosal blood flow in rats.

The effects of nicotine microinjected into several brain regions on the centrally elevated gastric acid output and mucosal blood flow (MBF) were examined in anesthetized rats. Intravenous administration of 2-deoxy-D-glucose (2-DG) induced increases in gastric acid output and MBF. These increases were inhibited dose dependently by nicotine microinjected into the dorsal motor nucleus of the vagus (NDV) but not into various hypothalamic regions. This effect of nicotine was abolished with concomitantly administered hexamethonium and was not observed in reserpine-pretreated animals. Electrical stimulation of the lateral hypothalamic area (LHA) induced an increase in gastric acid output. This increase was completely inhibited when nicotine was microinjected into the NDV 5 min before stimulation. This inhibitory effect of nicotine was abolished by concomitantly administered hexamethonium and by intraventricular pretreatment with phentolamine, but not with propranolol. These results suggest that activation of nicotinic receptors within the NDV releases noradrenaline and that there is a resultant inhibition of gastric acid output and MBF.

Animals↗

PubMed1986

KCl-induced calcium-independent release of endogenous dopamine from rat brain slices.

Effects of the absence of calcium on the KCl- and electrical stimulation-induced releases of endogenous dopamine (DA) from rat brain slices were studied and the findings were compared with the effects on the release of endogenous noradrenaline (NA). DA and NA were extracted by the aluminum-adsorption method and assayed electrochemically by high-performance liquid chromatography. KCl, 15 mM, induced a significant increase in the release of DA from both the striatum and the hypothalamus, even in the Ca2+-free medium containing 1 mM EGTA. In the normal medium, the KCl-induced release of DA was concentration-dependent (15, 30 and 50 mM), while that in the Ca2+-free medium showed a plateau at 30 mM of KCl. The release of DA induced by electrical stimulation (10 cycles/s, 2 ms, 30 mA, for 5 min) was abolished in the Ca2+-free medium as was NA induced by both KCl and electrical stimulation. Nomifensine, 10 microM, a DA transport inhibitor, abolished the 15 mM KCl-induced release of DA in the Ca2+-free medium. On the other hand, the release of DA induced by electrical stimulation was considerably enhanced by nomifensine. Therefore, the mode of DA release induced by KCl sometimes differed from that induced by electrical stimulation. The present results also suggest that DA released by KCl in the Ca2+-free medium originates from cytoplasmic DA storage sites, through a carrier-mediated process.

Animals↗

PubMed1986

Central cholinergic descending pathway to the dorsal motor nucleus of the vagus in regulation of gastric functions.

A possible role of the cholinergic mechanism within the dorsal motor nucleus of the vagus (NDV) in the regulation of gastric functions was examined in urethane anesthetized rats. Pretreatment with atropine (1-5 nmole), intracerebroventricularly inhibited the increase in both gastric acid output and mucosal blood flow (MBF), as induced by electrical stimulation of the lateral hypothalamic area (LHA). Bethanechol, microinjected into the dorsal vagal complex (the NDV, the nucleus tractus solitarius and area postrema) induced dose-dependent (5-30 nmole) increases in gastric acid output and MBF, while nicotine was without effect. Pretreatment with atropine 3 nmole microinjected into the dorsal vagal complex completely blocked the increases induced by electrical stimulation of the LHA. Furthermore, the increases in these gastric parameters induced by the administration of 2-deoxy-D-glucose (2-DG) were also significantly inhibited by atropine microinjected into the dorsal vagal complex. These results suggest that neurotransmission of the central descending pathway to the NDV in excitatory regulation of gastric functions is probably mediated through cholinergic muscarinic receptors.

Animals↗

PubMed1986

Lack of direct splanchnic nerve inhibitory effects on histamine-induced gastric acid secretion in rats.

Effects of stimulation of the splanchnic nerves (gastric sympathetic nerves) on the histamine-induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats. The gastric acid secretion and MBF were increased by i.v. infusion of a submaximal dose of histamine (50 micrograms/kg/min). Stimulation of the splanchnic nerve, carried out under an increased steady state of acid secretion and MBF, inhibited the histamine-induced acid secretion and MBF and these effects were abolished by phentolamine and augmented by propranolol. The manner of inhibition by splanchnic nerve stimulation was similar to the inhibitory effects of vasopressin on histamine-induced acid secretion and MBF, but differed from the inhibitory effects of somatostatin; i.v. infusion of vasopressin reduced both histamine-induced acid secretion and MBF, whereas i.v. infusion of somatostatin reduced the histamine-induced acid secretion more effectively than MBF. Inhibitory effects of splanchnic nerve stimulation or infusion of vasopressin on the histamine-induced gastric acid secretion and MBF paralleled the increases in the systemic blood pressure during such treatment. These results suggest that the splanchnic nerves have no direct inhibitory effect on the histamine-induced gastric acid secretion in rats. Decreases in the histamine-induced gastric acid secretion are probably secondary to the decrease in the MBF during splanchnic nerve stimulation.

Animals↗

PubMed1986

Alpha-1 adrenoceptors mediate splanchnic nerve inhibition of pentagastrin-induced gastric acid secretion and mucosal blood flow in rats.

Effects of stimulation of the sympathetic nervous system on pentagastrin-induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. Gastric acid secretion and MBF were increased by i.v. infusion of a submaximal dose of pentagastrin (1.0 microgram/kg/min). Stimulation of the splanchnic nerve was carried out under the steady, increased state of pentagastrin-stimulated acid secretion and MBF. Stimulation of the splanchnic nerve significantly reduced gastric acid secretion, while MBF was little affected. Thus, the delta MBF/delta H+ ratio was significantly increased during this stimulation. Phentolamine, but not propranolol, abolished the inhibitory effects of splanchnic nerve stimulation on the pentagastrin-stimulated gastric acid secretion. In addition, prazosin, but not yohimbine, abolished the inhibitory effects of splanchnic nerve stimulation on the pentagastrin-induced gastric acid secretion. These results suggest that splanchnic nerves directly inhibit pentagastrin-induced gastric acid secretion through alpha-1 adrenoceptors, independently of changes in the MBF, in rats.

Animals↗

PubMed1985

Cholecystokinin intracerebroventricularly applied stimulates gastric acid secretion.

Intracerebroventricularly applied cholecystokinin-8-sulfate (CCK-8) induced a significant and dose-related increase in gastric acid output in urethane anesthetized rats. On the other hand, cholecystokinin-8-non-sulfate (CCK-8-NS), a non-active analogue of CCK-8, and pentagastrin as one of the cholecystokinin families, had no effect on gastric acid secretion. Pretreatment with atropine 5 min prior to CCK-8 as well as subdiaphragmatic vagotomy completely blocked this peptide-induced increase in gastric acid secretion. These results suggest that centrally applied CCK-8 induced a vagally mediated increase in gastric acid secretion.

Animals↗

PubMed1985

A case of prostatic carcinoma with skin metastases.

The 30th case of metastatic skin carcinoma of prostatic origin was presented. The cytosolic R1881 receptor was detected moderately in the metastatic nodule of the skin, however, the measurement of this receptor had a limited value for the purpose of treating the patient with antiandrogenic agents.

Adenocarcinoma↗

PubMed1985

Effect of d-nicotine on the l-nicotine-induced increase in gastric acid secretion in rats.

d-Nicotine (1000 micrograms) applied into the cerebral ventricle of urethane anesthetized rats increased gastric acid secretion. When 50 micrograms of d-nicotine was concomitantly administered with 5 micrograms of 1-nicotine, the 1-nicotine-induced increases in gastric secretion was blocked. The appearance of convulsion induced by I-nicotine in mice was also inhibited by pretreatment with d-nicotine. These results suggest that d-nicotine has agonistic and antagonistic actions to I-nicotine in the central nervous system and that its agonistic potency varies with preparations.

Animals↗