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Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 91 records · Page 5Linked to original sources
PubMed1994

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes.

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes is reported. The etiology was considered to be the partial dysfunction of efferent sympathetic nerve endings. Peripheral adrenergic receptors (alpha and beta) were up-regulated, which might have caused pseudoischemic electrocardiographic changes and abnormal vasodilation after exercise.

Autonomic Nervous System Diseases↗
PubMed1994

Angiotensin II subtype 1 receptor modulates epinephrine release from isolated rat adrenal gland.

To elucidate the role of subtypes of the angiotensin (AT) II receptor in epinephrine release from the adrenal gland, the effects of AT II subtype 1 (AT1) receptor and AT II subtype 2 (AT2) receptor antagonists on AT II-induced modulation of epinephrine release were examined. Seven-week-old Wistar rats were used in this study. The left adrenal gland was perfused in a retrograde fashion. The effects of AT II on basal epinephrine release and epinephrine release by electrical stimulation were examined before and after treatment with CV-11974 (CV), an AT1 receptor antagonist, or PD123319 (PD), an AT2 receptor antagonist. AT II increased epinephrine release from the adrenal gland. CV almost completely suppressed AT II-induced increases in epinephrine release. In contrast, PD had no significant effects on AT II-induced increases in epinephrine release. These results suggest that AT II increases epinephrine release from the adrenal medulla via the AT1 receptor.

Adrenal Glands↗
PubMed1994

Glutamatergic regulation of [3H]-noradrenaline release in the medulla oblongata of normotensive and spontaneously hypertensive rats.

OBJECTIVE: To assess in vitro the role of glutamate receptors in the regulation of noradrenaline release from the medulla oblongata of normotensive and hypertensive rats. DESIGN AND METHODS: The effects of L-glutamate (an endogenous ligand for glutamate receptors), glycine (an allosteric agonist for the N-methyl-D-aspartate type of glutamate receptors) and MK-801 (an antagonist for N-methyl-D-aspartate receptors) on [3H]-noradrenaline release were examined in slices of rat medulla oblongata. RESULTS: L-Glutamate elicited [3H]-noradrenaline release from slices of rat medulla oblongata in magnesium-free medium. Glycine also increased the release of noradrenaline. Moreover, the effect of L-glutamate on noradrenaline release was significantly potentiated by glycine. MK-801 inhibited the increase in noradrenaline release evoked by L-glutamate. In spontaneously hypertensive rats (SHR) the facilitatory effect of L-glutamate on noradrenaline release was significantly more pronounced than in Wistar-Kyoto (WKY) rats. Furthermore, glycine alone and in combination with L-glutamate increased the noradrenaline release to a greater extent in SHR than in WKY rats. CONCLUSION: The present results show that the excitatory amino acids might increase noradrenaline release from rat medulla oblongata, which was partially dependent on the N-methyl-D-aspartate type of glutamate receptors. The greater effect of L-glutamate and glycine in SHR suggests that these amino acids might be involved in the regulation of noradrenaline release in the medulla oblongata of hypertension.

Animals↗
PubMed1994

[A resected case of sporadic myxoma of the right ventricle: the diagnosis was supported with DNA flow cytometry].

We report a rare case of a 16-year-old male who had myxoma originating from septal band of the right ventricle. His ECG anomaly was found incidentally upon a physical examination. Subsequently, echocardiography and angiocardiography demonstrated a tumor occupying the right ventricular outflow tract and protruding into the main pulmonary artery in systolic phase. He was operated upon using extracorporeal circulation. By right ventriculotomy the tumor was resected together with septal tissue 5 mm around the stalk, which branched into the myocardium. The defect was closed using mattress sutures with Dacron felt strips. We also analyzed the DNA content of the tumor. The DNA flow cytometry yielded a single cell population with diploid DNA content. This result showed that the tumor is sporadic form of cardiac myxoma. His postoperative course was uneventful. Thirty months after the surgery, patient has no sign of recurrence. The DNA flow cytometry is helpful for detecting clinical behavior of the cardiac myxoma, because microscopic examination can not readily distinguish sporadic myxoma from so-called complex myxoma.

Adolescent↗
PubMed1993

Production of nerve growth factor by cultured vascular smooth muscle cells from spontaneously hypertensive and Wistar-Kyoto rats.

OBJECTIVE: Nerve growth factor (NGF) is a neurotrophic protein which acts on peripheral sympathetic nerves. Elevated NGF in vascular tissues of young spontaneously hypertensive rats (SHR) has been reported. The aim of the present study was to compare the amount of NGF secreted from cultured vascular smooth muscle cells (VSMC) and mesenteric artery and thoracic aorta segments from SHR and Wistar-Kyoto (WKY) rats. METHODS: VSMC prepared by the enzyme digestion method from the thoracic aortic media of 14-week-old SHR and age-matched WKY rats were subcultured in Dulbecco's modified Eagle's medium containing 10% fetal calf serum. Segments of mesenteric artery and thoracic aorta from 4-week-old SHR and age-matched WKY rats were similarly cultured. The NGF content in conditioned medium was measured using an enzyme immunoassay. The protein content of VSMC was measured by the Lowry method. RESULTS: Total NGF content in the cell culture medium was increased during an exponential growth phase and then gradually decreased during a quiescent phase in both rat strains. There were no significant differences in the levels of NGF secreted from mesenteric artery and thoracic aorta segments between the SHR and WKY rats. The differences in cellular protein content between SHR and WKY rats were very small. CONCLUSIONS: In contrast to the reports of increased NGF in SHR tissues, our data demonstrate that NGF secretion was lower in VSMC from SHR, and was equivalent in mesenteric artery and thoracic aorta segments from SHR and WKY rats. We have no clear explanation for these observations, but the present results indicate that upregulation of NGF in SHR tissues is not responsible for a simple enhancement of NGF synthesis in VSMC, and suggest a breakdown of the regulatory mechanism or mechanisms of NGF gene expression in SHR tissues.

Animals↗
PubMed1993

Effects of bradykinin on [3H]-norepinephrine release in rat hypothalamus.

1. We examined the regulatory actions of bradykinin on norepinephrine release in the hypothalamus of rats. 2. Bradykinin increased the stimulation-evoked [3H]-norepinephrine release from hypothalamic slices of Sprague-Dawley rats in a dose-dependent manner (1 Hz: S2/S1 ratio, mean +/- s.e.m., control 0.868 +/- 0.016, n = 6; bradykinin 1 x 10(-6) mol/L 1.039 +/- 0.018, n = 6, P < 0.05; bradykinin 3.3 x 10(-6) mol/L 1.130 +/- 0.064, n = 6, P < 0.05). The basal release of [3H]-norepinephrine was not affected by the peptide. 3. Bay K 8644, a dihydropyridine-sensitive calcium channel agonist, significantly potentiated the facilitatory effect of bradykinin on norepinephrine release, although Bay K 8644 by itself had no significant effect. By contrast, nicardipine, a dihydropyridine-sensitive calcium channel blocker, reversed the increase in norepinephrine release induced by bradykinin and Bay K 8644. 4. These results indicate that bradykinin may increase norepinephrine release in rat hypothalamus, partially mediated by interactions with dihydropyridine-sensitive calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Effects of nicardipine on the release of acetylcholine in the rat central nervous system.

Recent studies have indicated that specific dihydropyridine-sensitive Ca2+ channel binding sites are present in the brain, and that they play a crucial role in synaptic function. The present study was performed to determine the effects of nicardipine, a dihydropyridine-sensitive Ca2+ channel blocker, on the release of acetylcholine in the rat central nervous system. Striatal slices of rats which had been prelabelled with [3H]acetylcholine were superfused with Krebs-Ringer solution. The slices were stimulated with either electrical pulses (1 Hz) or an excitatory amino acid, L-glutamate, and the effects of nicardipine on the release of acetylcholine were examined. Electrical stimulation produced an increase in [3H]acetylcholine release from the striatal slices. Exposure of the slices to nicardipine significantly inhibited the stimulation-evoked [3H] acetylcholine release. An endogenous excitatory amino acid, L-glutamate, also elicited release of [3H]acetylcholine. Nicardipine significantly reduced the L-glutamate-induced release of [3H]acetylcholine, and the effect was pronounced in the presence of Mg2+. These results demonstrate that nicardipine inhibits both electrically and chemically stimulated [3H]acetylcholine release from rat striatum. The ability of nicardipine to inhibit cholinergic transmission may be related to the central effect of this Ca2+ channel blocker.

Acetylcholine↗
PubMed1993

Membrane fluidity of erythrocytes and its modulation by ouabain in essential hypertension--an electron paramagnetic resonance study.

The purpose of the present study was to examine alterations in membrane fluidity of erythrocytes in essential hypertension by means of an electron paramagnetic resonance (EPR) and a spin labeling method. In addition, we investigated the effects of ouabain on the fluidity of erythrocytes, and elucidated a possible role of Na+, K(+)-ATPase in the regulation of membrane fluidity in hypertension. Erythrocytes obtained from patients with essential hypertension were examined compared with those from age-matched normotensive subjects. The EPR spectra for 5-nitroxide stearate incorporated into erythrocyte membranes were studied. The values of the outer hyperfine splitting and order parameter (S) of the EPR spectra were significantly higher in patients with essential hypertension than in normotensive subjects. This finding shows that the membrane fluidity of erythrocytes might be lower in essential hypertension. Ouabain-loading of erythrocytes decreased the membrane fluidity (S value was increased). The ouabain-induced changes were significantly greater in essential hypertension than in normotensive subjects. These results demonstrate that the membrane fluidity of erythrocytes might be lower in essential hypertension than in normotensive subjects. Furthermore, the membrane fluidity might be highly dependent on the Na+, K(+)-ATPase activity in essential hypertension, which would suggest an abnormality in Na(+)-related cellular functions in hypertension.

Electron Spin Resonance Spectroscopy↗
PubMed1993

[The effects of anesthetic techniques and insufflating gases on ventilation during laparoscopy].

The present study was performed to clarify the influences of anesthetic methods and insufflating gases on arterial blood gas and ventilation during laparoscopy. Forty five women undergoing laparoscopy for gynecological procedure were studied after dividing into four groups; general anesthesia with control ventilation or epidural anesthesia with spontaneous breathing, plus insufflation with carbon dioxide (CO2) or nitrous oxide (N2O). After CO2 insufflation, PaCO2 increased significantly in the patients who were mechanically ventilated, but not in the patients breathing spontaneously. After N2O insufflation, the decrease in tidal volume (VT) and the increase in VD/VT were significant, but minute ventilation was well maintained by the compensatory increase in respiratory frequency during spontaneous breathing. On the other hand, after CO2 insufflation VE and VD/VT increased significantly without any change in VT. PaO2 decreased significantly after both insufflation and Trendelenburg tilt in all groups, probably secondary to the decrease in functional residual capacity. These findings suggest that during laparoscopy, ventilation could be well maintained by spontaneous breathing, although the increase in VD/VT and costal breathing indicate the increase in respiratory work load. We recommend that ventilation and oxygenation should be closely monitored during laparoscopy to avoid hypercapnia and hypoxia.

Adolescent↗
PubMed1993

[Effect of succinylcholine on serum potassium concentration in children with chronic renal failure].

Serum potassium (K+) levels were measured after intravenous injection of succinylcholine (SCh) in 10 children with chronic renal failure, 10 normal children aged 1 to 10 years and 10 children with chronic renal failure after pretreatment with pancuronium prior to SCh. Arterial blood gas was maintained within normal ranges. The serum K+ level increased significantly during 10 minutes after SCh in normal children. There was no significant difference between serum K+ levels in normal children and those in children with chronic renal failure. Administration of pancuronium in small doses (20 micrograms.kg-1) prior to SCh (1 mg.kg-1) was not effective to prevent serum K+ elevation completely. Our results indicate that the administration of SCh in children with chronic renal failure might be possible without increasing serum potassium level.

Child↗
PubMed1992

Facilitatory effects of diltiazem on dopamine release in the central nervous system. Focus on interactions with D2 autoreceptors and guanosine triphosphate binding proteins.

The purpose of the present study was to investigate the effects of a Ca antagonist (diltiazem) on dopamine release in the central nervous system. Rat striatal slices prelabeled with [3H]dopamine (DA) and superfused with Krebs-Ringer solution were stimulated electrically at a frequency of 1 Hz. Exposure to diltiazem (3.3 x 10(-7) to 1 x 10(-5) mol/L) significantly increased both the basal and stimulation-evoked [3H]DA release in a dose-dependent manner. Exogenously applied unlabeled DA inhibited the stimulation-evoked [3H]DA release. Diltiazem significantly antagonized the capacity of the unlabeled DA to inhibit stimulation-evoked [3H]DA release. The blockade of D2 receptors by a preferential D2 antagonist, sulpiride, reduced the facilitatory effect of diltiazem on stimulation-evoked [3H]DA release. Pretreatment with pertussis toxin, which interferes with the coupling of the inhibitory guanosine triphosphate-binding proteins to adenylate cyclase, significantly diminished the effects of diltiazem on stimulation-evoked [3H]DA release. These results show that diltiazem increased DA release in rat striatum, at least partially by interactions with the D2 autoreceptors and pertussis toxin-sensitive guanosine triphosphate-binding proteins.

Adenylate Cyclase Toxin↗
PubMed1992

Increased nerve growth factor levels in spontaneously hypertensive rats.

OBJECTIVE: Increased sympathetic innervation has been reported in spontaneously hypertensive rats (SHR); however, the precise mechanisms involved are not yet clear. Nerve growth factor (NGF), a neurotrophic peptide in peripheral sympathetic neurons, is believed to contribute to this phenomenon. METHODS: We measured the content of NGF in SHR and control Wistar-Kyoto (WKY) rats during development. Mesenteric artery, spleen, heart and sciatic nerve were isolated and homogenized. NGF content in the supernatant fractions was measured using a highly sensitive and specific two-site enzyme immunoassay. RESULTS: At 3 weeks of age, SHR had a greater NGF content in the spleen, the sciatic nerve and the mesenteric artery than WKY rats. However, these differences disappeared completely at 12 weeks of age. Cardiac NGF content was slightly lower in 3-week-old SHR and, conversely, higher in 12-week-old SHR than in age-matched WKY rats. CONCLUSIONS: These findings suggest that, except for the heart, the SHR tissues observed overproduce NGF at a young age, leading to enhancement of peripheral sympathetic nervous system activity and the production of vasoconstrictive catecholamines.

Aging↗
PubMed1992

Presynaptic alpha 2-adrenoceptor-mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats.

The present study was designed to investigate the presynaptic alpha 2-adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na-loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na-loaded HT and normotensive control rats (NT-control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na-loaded HT than in NT-control. Yohimbine, a potent alpha 2-adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na-loaded HT compared with NT-control. These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na-loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na-loaded HT could partially depend on impaired presynaptic alpha 2-adrenoceptor-mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt-dependent hypertension.

Animals↗
PubMed1992

Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus.

In the present study, we examined the regulatory mechanisms of calcitonin gene-related peptide on norepinephrine release in rat hypothalamus. Calcitonin gene-related peptide inhibited the stimulation-evoked norepinephrine release from hypothalamic slices of Sprague-Dawley rats in a dose-dependent manner, although the peptide did not affect basal release of norepinephrine. The blockade of the alpha 2-adrenergic receptors by RX 781094 failed to modulate the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. Pretreatment of slices with islet activating protein, a toxin that interferes with the coupling of the inhibitory receptors to adenylate cyclase, did not affect the suppression of norepinephrine release by calcitonin gene-related peptide. However, Bay K 8644, a dihydropyridine-sensitive calcium channel agonist, significantly reversed the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. These results show that calcitonin gene-related peptide might inhibit norepinephrine release in rat hypothalamus, partially mediated by interactions with dihydropyridine-sensitive Ca2+ channels but not by interactions with presynaptic alpha 2-adrenergic receptors and inhibitory guanosine triphosphate binding proteins. Furthermore, the finding suggests the possible involvement of calcitonin gene-related peptide in the regulation of sympathetic nervous activity in the central nervous system.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Modulation of norepinephrine release by galanin in rat medulla oblongata.

Galanin, a 29-amino acid peptide, is widely distributed in both the central and peripheral nervous systems and is colocalized with catecholamines, although its physiological significance remains to be elucidated. In the present study we investigated the regulatory mechanisms of galanin on norepinephrine release in rat medulla oblongata. In slices of medulla oblongata of Sprague-Dawley rats, galanin inhibited the stimulation-evoked [3H]norepinephrine release in a concentration-dependent manner (fractional release ratio during electrical stimulation: control 0.937 +/- 0.043, mean +/- SEM, n = 6; galanin 1 x 10(-7) M 0.501 +/- 0.037, n = 6, p less than 0.05; and galanin 1 x 10(-6) M 0.299 +/- 0.018 n = 6, p less than 0.05). Galanin potentiated inhibition of [3H]norepinephrine release by the alpha 2-agonists (UK 14,304 and clonidine). The blockade of alpha 2-adrenergic receptors by RX 781094 diminished the inhibition of norepinephrine release by galanin. Pretreatment of pertussis toxin, which interferes with the coupling of inhibitory guanosine triphosphate-binding proteins to adenylate cyclase, significantly attenuated the suppressive effects of galanin on norepinephrine release. In slices of medulla oblongata obtained from spontaneously hypertensive rats (SHR), the inhibitory effect of galanin on norepinephrine release was significantly less than in those from age-matched Wistar-Kyoto rats. These results show that galanin might inhibit the stimulation-evoked norepinephrine release in rat medulla oblongata, at least partially mediated by alpha 2-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins. Moreover, less suppression of norepinephrine release by galanin in SHR suggests that galanin might be involved in the regulation of central sympathetic nervous activity in hypertension.

Adenylate Cyclase Toxin↗
PubMed1992

Modulation of noradrenergic transmission by neuropeptide Y and presynaptic alpha 2-adrenergic receptors in the hypothalamus of spontaneously hypertensive rats.

Neuropeptide Y (NPY) has a wide and specific distribution in the central nervous system, and is colocalized with catecholamines in specific neuronal systems. In this study, in order to investigate the regulatory mechanisms of NPY and presynaptic alpha 2-adrenergic receptors on central noradrenergic transmission in hypertension, we have examined the effects of NPY and the alpha 2-agonist, UK 14,304, on (3H)-noradrenaline (NA) release from hypothalamic slices of spontaneously hypertensive rats (SHR). Electrical stimulation (1 Hz)-evoked (3H)-NA release was significantly greater in the hypothalamic slices of SHR than in those of Wistar Kyoto rats (WKY). NPY and the alpha 2-agonist, UK 14,304, inhibited the stimulation-evoked (3H)-NA release in a dose-related manner. The inhibitory effects of NPY and UK 14,304 on NA release were significantly attenuated in SHR compared with WKY. These results suggest that NPY and alpha 2-adrenoceptors might be involved in the regulation of central sympathetic nervous activity in hypertension.

Adrenergic alpha-Agonists↗