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Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 19 recordsLinked to original sources
PubMed2001

Hyperinsulinemia is a determinant of membrane fluidity of erythrocytes in essential hypertension.

In the present study, to determine a possible role of insulin in the regulation of membrane functions, we have examined the relationship between plasma insulin level and membrane fluidity of erythrocytes in patients with essential hypertension and normotensive subjects. Membrane fluidity of erythrocytes obtained from hypertensive and normotensive subjects were evaluated by means of an electron paramagnetic resonance and spin-labeling method. The order parameter (S for 5-nitroxide stearate) and the peak height ratio (ho/h(-1) for 16-nitroxide stearate) obtained from electron paramagnetic resonance spectra of erythrocyte membranes were significantly higher in patients with essential hypertension than in normotensive subjects. The finding indicated that the erythrocyte membrane fluidity was lower in essential hypertension than in normotensive controls. The plasma concentration of insulin while fasting was also significantly greater in hypertensive patients than in normotensive subjects. In addition, the plasma insulin level was significantly correlated with the values of the order parameter (S) and the peak height ratio (ho/h(-1)), which showed that the higher plasma insulin was associated with the lower membrane fluidity of erythrocytes. These results support the hypothesis that insulin may actively participate in the regulation of membrane fluidity of erythrocytes in essential hypertension.

Blood Pressure↗
PubMed2001

Bone mineral density in women with essential hypertension.

Recent studies have reported the abnormalities in calcium metabolism at the systemic level in human hypertension as well as in experimental hypertension. Because bone is the largest store of calcium in the body, the bone calcium content and mineralization may represent the entire calcium balance. The present study was undertaken to investigate the bone mineral density (BMD) in women with essential hypertension by means of the dual-energy X-ray absorptiometric (DXA) method. The DXA analysis showed a significant decrease in BMD in female hypertensive subjects compared with normotensive subjects. In addition, the BMD was inversely correlated with systolic blood pressure in women. The 24-h urinary calcium excretion was significantly greater in female hypertensive subjects than in female normotensive subjects. Furthermore, the greater the urinary calcium excretion, the lower the BMD in women. The values of serum total calcium, total magnesium, ionized calcium, and 1, 25(OH)2 vitamin D were not different between hypertensive and normotensive subjects. The results of the present study demonstrated that DXA provided an index of whole calcium balance, and suggest that high blood pressure might be associated with reduced BMD in female hypertension.

Absorptiometry, Photon↗
PubMed2001

Role of dihydropyridine-sensitive calcium channels in the regulation of norepinephrine release in hypertension.

In the present study, in order to elucidate the role of dihydropyridine (DHP)-sensitive calcium (Ca) channels in the regulation of neurotransmitter release in hypertension, we examined the effects of the DHP-sensitive Ca channel blocker nicardipine on norepinephrine (NE) release in blood vessels of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The stimulation-evoked pressor responses and NE release were significantly greater in the mesenteric arteries of SHR than in the mesenteric arteries of WKY rats. Nicardipine significantly inhibited the stimulation-evoked NE release as well as vasoconstrictor responses in the mesenteric arteries to a greater extent in SHR than in WKY rats. These results demonstrated that nicardipine markedly reduced the stimulation-evoked NE release in blood vessels of SHR, which might suggest that the DHP-sensitive Ca channels could be involved, at least in part, in the regulation of NE release in hypertension.

Animals↗
PubMed2001

Electron paramagnetic resonance investigation on modulatory effect of 17beta-estradiol on membrane fluidity of erythrocytes in postmenopausal women.

Many studies have shown that estrogen may exert cardioprotective effects and reduce the risk of hypertension and coronary events. On the other hand, it has been proposed that cell membrane abnormalities play a role in the pathophysiology of hypertension, although it is not clear whether estrogen would influence membrane function in essential hypertension. The present study was performed to investigate the effects of 17beta-estradiol (E(2)) on membrane fluidity of erythrocytes in normotensive and hypertensive postmenopausal women. We determined the membrane fluidity of erythrocytes by means of an electron paramagnetic resonance and spin-labeling method. In an in vitro study, E(2) significantly decreased the order parameter for 5-nitroxide stearate and the peak height ratio for 16-nitroxide stearate obtained from electron paramagnetic resonance spectra of erythrocyte membranes in normotensive postmenopausal women. The finding indicates that E(2) might increase the membrane fluidity of erythrocytes. The effect of E(2) was significantly potentiated by the NO donor, S-nitroso-N-acetylpenicillamine, and a cGMP analogue, 8-bromo-cGMP. In contrast, the change in the membrane fluidity evoked by E(2) was attenuated in the presence of the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester, and asymmetric dimethyl-L-arginine. In hypertensive postmenopausal women, the membrane fluidity of erythrocytes was significantly lower than that in normotensive postmenopausal women. The effect of E(2) on membrane fluidity was significantly more pronounced in the erythrocytes of hypertensive postmenopausal women than in the erythrocytes of normotensive postmenopausal women. The results of the present study showed that E(2) significantly increased the membrane fluidity and improved the microviscosity of erythrocyte membranes, partially mediated by an NO- and cGMP-dependent pathway. Furthermore, the greater action of E(2) in hypertension might be consistent with the hypothesis that E(2) could have a beneficial effect in regulating rheological behavior of erythrocytes and could have a crucial role in the improvement of the microcirculation in hypertension.

Aged↗
PubMed2001

Estriol improves membrane fluidity of erythrocytes by the nitric oxide-dependent mechanism: an electron paramagnetic resonance study.

The present in vitro study was performed to investigate the effects of estriol (E3) on membrane fluidity of erythrocytes by means of an electron paramagnetic resonance (EPR) and spin-labeling method. E3 was shown to significantly decrease the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (ho/h-1) for 16-NS obtained from EPR spectra of erythrocyte membranes. This finding indicated that E3 might increase the membrane fluidity of erythrocytes. The effect of E3 was significantly potentiated by the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and a cyclic guanosine 3',5'-monophosphate (cGMP) analog, 8-bromo-cGMP. In contrast, the change in the membrane fluidity induced by E3 was antagonized by the NO synthase inhibitor, L-NG-nitroarginine-methyl-ester (L-NAME), and asymmetric dimethyl-L-arginine (ADMA). The results of the present study showed that E3 significantly increased the membrane fluidity and improved the microviscosity of erythrocyte membranes, partially mediated by an NO- and cGMP-dependent pathway. Furthermore, the data might be consistent with the hypothesis that E3 could have a beneficial effect on the rheological behavior of erythrocytes and may play a crucial role in the regulation of microcirculation.

Arginine↗
PubMed2000

Nitric oxide improves membrane fluidity of erythrocytes in essential hypertension: An electron paramagnetic resonance investigation.

It has been shown that rheological abnormality might be an etiological factor in hypertension. Recent studies have revealed that human erythrocytes possess a nitric oxide (NO) synthase and that this activation might be involved in the regulation of rheological properties of erythrocytes. The present study was undertaken to investigate the role of NO in the regulation of membrane functions of erythrocytes in patients with essential hypertension by means of an electron paramagnetic resonance (EPR) and spin-labeling method. The NO donor S-nitroso-N-acetylpenicillamine (SNAP) decreased the order parameter (S) for 5-nitroxide stearate (5-NS) and the peak height ratio (h(0)/h(-1)) for 16-NS obtained from EPR spectra of erythrocyte membranes in a dose-dependent manner. The finding indicated that the NO donor increased the membrane fluidity of erythrocytes. In addition, the effect of SNAP was significantly potentiated by 8-bromo-cyclic guanosine monophosphate. By contrast, the change of the fluidity induced by SNAP was reversed in the presence of L-N(G)-nitroarginine methyl ester and asymmetric dimethyl L-arginine. In patients with essential hypertension, the membrane fluidity of erythrocytes was significantly lower than in the normotensive subjects. The effect of SNAP was more pronounced in essential hypertension than in normotensive subjects. These results showed that NO increased the membrane fluidity and decreased the rigidity of cell membranes. Furthermore, the greater effect of NO on the fluidity in essential hypertension suggests that NO might actively participate in the regulation of rheological behavior of erythrocytes and have a crucial role in the improvement of microcirculation in hypertension.

Arginine↗
PubMed2000

Regio- and diastereocontrol in carbonyl allylation by 1-halobut-2-enes with Tin(II) halides

Regio- and diastereoselective carbonyl allylations of 1-halobut-2-enes with tin(II) halides are described. Tin(II) bromide in a dichloromethane-water biphasic system is an effective reagent for unusual alpha-regioselective carbonyl allylation of 1-bromobut-2-ene to produce 1-substituted pent-3-en-1-ols. The addition of tetrabutylammonium bromide (TBABr) to the biphasic system produces 1-substituted 2-methylbut-3-en-1-ols via usual gamma-addition which is opposite to the alpha-addition without TBABr. The gamma-addition to aromatic aldehydes exhibits anti-diastereoselectivity, while that to aliphatic aldehydes is not diastereoselective. The allylation of benzaldehyde by 1-chlorobut-2-ene in 1,3-dimethylimidazolidin-2-one (DMI) does not occur with tin(II) chloride or bromide but does proceed with tin(II) iodide and exhibits gamma-syn selectivity which is unusual for a Barbier-type carbonyl allylation. In the carbonyl allylation by 1-chlorobut-2-ene with any tin(II) halide, the addition of tetrabutylammonium iodide (TBAI) accelerates the reaction and enhances gamma-syn selectivity. The use of tin(II) iodide and TBAI produces 2-methyl-1-phenylbut-3-en-1-ol with high yield and high syn-diastereoselectivity. The syn-diastereoselective carbonyl allylation of 1-chlorobut-2-ene using tin(II) iodide, a catalytic amount of TBAI, and NaI in DMI-H(2)O is applied to various aldehydes.

Journal Article↗
PubMed2000

Role of insulin in the regulation of membrane fluidity of erythrocytes in essential hypertension: an electron paramagnetic resonance investigation.

In the present study, to determine a possible role of insulin in the regulation of membrane functions, we have examined the effects of insulin on the membrane fluidity of erythrocytes in patients with essential hypertension and normotensive subjects. Membrane fluidity of erythrocytes obtained from hypertensive and normotensive subjects were evaluated by means of an electron paramagnetic resonance (EPR) and a spin-labeling method. In an in vitro study, insulin increased the order parameter (S for 5-nitroxide stearate) and the peak height ratio (ho/h-1 for 16 nitroxide stearate) in the EPR spectra of erythrocyte membranes, which indicated that insulin decreased the membrane fluidity of erythrocytes. The effects of insulin on the membrane fluidity were potentiated in the presence of extracellular Ca2+, and in contrast, were antagonized by the Ca2+ channel blocker diltiazem. Furthermore, the effects of insulin alone and in combination with Ca2+ on the membrane fluidity were reduced in the erythrocytes from hypertensive subjects compared with the erythrocytes from normotensive controls. The high concentrations of glucose alone produced no significant effects on the membrane fluidity of erythrocytes. These results demonstrated that insulin might actively participate in the regulation of membrane fluidity of erythrocytes, which might be mediated by the intracellular Ca2+ kinetics.

Calcium↗
PubMed2000

Effects of beta-endorphin on norepinephrine release in hypertension.

Recent studies have suggested an involvement of the endogenous opioid system in blood pressure control. The purpose of the present study was to determine the role of beta-endorphin in the regulation of sympathetic nervous activity in the central nervous system of hypertension. The effects of beta-endorphin on the electrically evoked release of [3H]norepinephrine (NE) were investigated in superfused slices of rat medulla oblongata. Beta-endorphin inhibited the stimulation-evoked NE release in a dose-dependent manner in rat medulla oblongata. In the medulla oblongata of spontaneously hypertensive rats (SHR), the inhibitory effect of beta-endorphin on the stimulation-evoked NE release was significantly smaller than in the medulla oblongata of Wistar-Kyoto rats. These results showed that beta-endorphin might reduce NE release in rat medulla oblongata. Furthermore, the lesser inhibitory effect of beta-endorphin on NE release in SHR might suggest that the opioid peptide could be involved in the regulation of central sympathetic nervous activity in hypertension.

Animals↗
PubMed1999

Histamine monoclonal antibody for brain immunocytochemistry.

Among five monoclonal antibodies (AHA-1 to 5 mAbs) prepared against glutaraldehyde (GA)-conjugated histamine (HA) in our previous study, only mAb AHA-2 was found to detect HA specifically in rat brain neurons by an immunocytochemistry method (ICC) using GA as a tissue fixative. All the other mAbs, except for AHA-5, reacted with HA in the enterochromaffin-like cells (ECL cells) of rat stomach [Fujiwara et al. (1997) Histochem. Cell Biol. 107, 39-45]. Enzyme-linked immunosorbent assay (ELISA) binding and inhibition tests demonstrated that AHA-2 is specific for HA, with almost no detectable cross-reaction with any other established or putative amino acid neurotransmitters, LH-RH, TRH, or peptides with N-terminal histidines. ELISA assays also suggested that the AHA-2 mAb recognizes a HA epitope structure different from the one recognized by the AHA-1 mAb. The immunostaining patterns with AHA-2 mAb, as seen in the five subgroups of the tuberomammillary nuclei in the rat posterior hypothalamus, were very similar to those described by Inagaki et al. [(1988) Brain Res. 439, 402-405; (1990) Exp. Brain Res. 80, 374-380] and Panula et al. [(1984) Proc. Natl. Acad. Sci. USA 81, 2572-2576; (1988) J. Histochem. Cytochem. 36, 259-269] using polyclonal anti-HA serum. However, it was also noted that moderate numbers of immunoreactive nerve fibers projected into the median eminence. The present HA ICC method using AHA-2 mAb allows highly sensitive HA detection in brain, and thus might permit detailed studies of HA localization hitherto impossible using previously available anti-HA polyclonal antibodies produced against carbodiimide-conjugated HA.

Animals↗
PubMed1999

Adrenomedullin and membrane fluidity of erythrocytes in mild essential hypertension.

OBJECTIVE: Adrenomedullin is a newly discovered 52 amino acid peptide that has a potent vasodilating action. The present study was undertaken to investigate the role of adrenomedullin in the regulation of membrane fluidity of erythrocytes in patients with essential hypertension. METHODS AND RESULTS: We used an electron paramagnetic resonance and spin-labeling method. Adrenomedullin significantly decreased the order parameter for 5-nitroxide stearate and peak height ratio for 16-nitroxide stearate obtained from electron paramagnetic resonance spectra of erythrocyte membranes in normotensive volunteers (mean +/- SEM order parameter value: control, 0.718 +/- 0.003, n = 16; adrenomedullin at 10(-9) mol/l, 0.692 +/- 0.004, n = 16, P < 0.05; adrenomedullin at 10(-8) mol/l, 0.690 +/- 0.004, n = 16, P < 0.05; adrenomedullin at 10(-7) mol/l, 0.683 +/- 0.004, n = 16, P < 0.05). The findings showed that adrenomedullin increased the membrane fluidity of erythrocytes. In addition, the effect of adrenomedullin was significantly potentiated by prostaglandin E1 and dibutyryl cyclic AMP. In contrast, the calcium ionophore A23187 counteracted the actions of adrenomedullin. In patients with essential hypertension, who had higher order parameter values, the membrane fluidity of erythrocytes was significantly lower than in the normotensive control subjects (order parameter: 0.728 +/- 0.004 in hypertensives, n = 20; 0.692 +/- 0.002 in normotensives, n = 36, P < 0.01). The effect of adrenomedullin on membrane fluidity was more pronounced in the erythrocytes of essential hypertensive than in the erythrocytes of normotensive subjects (change in the order parameter with adrenomedullin at 10(-9) mol/l: -4.2 +/- 0.3% in hypertensives, n = 20; -1.8 +/- 0.2% in normotensives, n = 20, P < 0.05; adrenomedullin at 10(-8) mol/l: -4.5 +/- 0.3% in hypertensives, n = 20; -1.8 +/- 0.2% in normotensives, n = 36, P < 0.05). CONCLUSIONS: The results of the present study demonstrate that adrenomedullin significantly increased the membrane fluidity of erythrocytes. The mechanisms were partially mediated by a prostaglandin E1- and cyclic AMP-dependent pathway which might be linked to changes in intracellular calcium kinetics. The greater effect of adrenomedullin in patients with essential hypertension suggests that the peptide might actively participate in the regulation of membrane functions in hypertension.

Adrenomedullin↗
PubMed1998

Effects of galanin on dopamine release in the central nervous system of normotensive and spontaneously hypertensive rats.

Galanin is a 29-amino acid peptide and widely distributed in the brain, although its significance in the control of neural activities is undefined. In the present study, we describe the effects of galanin on the electrically evoked release of dopamine in the rat central nervous system. In addition, to elucidate a possible role of galanin in the regulation of dopaminergic transmission in hypertension, we examined whether the effect of galanin on dopamine release might be altered in the central nervous system of spontaneously hypertensive rats (SHR). Galanin (1 x 10(-8) to 1 x 10(-7) mol/L) inhibited the stimulation (1 Hz)-evoked [3H]dopamine release by a comparable amount in striatal slices of Sprague-Dawley rats, although the basal release of dopamine was not affected by the peptide. In the striatum of SHR, the electrical stimulation (1 Hz)-evoked [3H]dopamine release was significantly smaller than in the striatum of Wistar-Kyoto (WKY) rats. However, the inhibitory effect of galanin on the stimulation-evoked [3H]dopamine release was significantly more pronounced in SHR than in WKY rats. These results show that galanin significantly reduced the release of dopamine in rat striatum. Furthermore, the greater inhibitory effect of galanin on dopamine release in SHR suggests that galanin might actively participate in the regulation of dopaminergic nerve activity in hypertension.

Animals↗
PubMed1998

Captopril inhibits both dopaminergic and cholinergic neurotransmission in the central nervous system.

1. The present study was performed to investigate the effects of captopril on both dopaminergic and cholinergic neurotransmission in the rat central nervous system. 2. Slices of rat striatum were prepared and prelabelled with [3H]-dopamine or [3H]-choline. Slices were continuously superfused with Krebs'-Ringer solution and electrical stimulation (1 Hz) was performed. 3. Captopril significantly inhibited stimulation-evoked [3H]-dopamine release from rat striatal slices in a concentration-dependent manner (S2/S1 ratios: control 0.835 +/- 0.018 (n = 6); 1 x 10(-5) mol/L captopril 0.597 +/- 0.035 (n = 6; P < 0.05); 5 x 10(-5) mol/L captopril 0.561 +/- 0.041 (n = 6; P < 0.05)). However, the basal release of [3H]-dopamine was not affected by captopril. 4. Captopril also reduced stimulation-evoked [3H]-acetylcholine release in the striatum (S2/S1 ratios: control 0.891 +/- 0.016 (n = 6); 1 x 10(-5) mol/L captopril 0.794 +/- 0.011 (n = 6; P < 0.05)). 5. These results show that captopril inhibits the release of both dopamine and acetylcholine in the rat striatum. Although the mechanisms underlying the neurosuppressive effects of captopril remain to be determined, the findings suggest that the inhibition of dopaminergic and cholinergic neurotransmission may be related to the central action of the angiotensin-converting enzyme inhibitor.

Acetylcholine↗
PubMed1998

Dietary balance chart for an on-line computerized graphical support system in MHTS.

Dietary habits are believed to play an important role in the etiology of adult disease. For this reason, it is necessary to include effective dietary guidance in multiphasic health testing and services (MHTS) programmes for primary disease prevention. We have developed such a programme of simple dietary advice, using a computer system for the MHTS. Examinees' dietary habits are checked using optical character record (OCR) questionnaire forms, and the results are displayed on the screen of a colour display terminal. They are required to prepare a menu of their usual daily dietary intake in terms of quantity and type of food. Thus the data collected relate to the nutritional composition of the examinee's usual diet. Nutritional requirements of the Japanese according to sex, height, and level of physical activity, in accordance with criteria set by the Japanese Ministry of Health and Welfare, are fed into the computer in advance. For each examinee, these criteria and the results of the assessment of the diet are displayed together on the screen in the form of colour graphs for comparison.

Adult↗
PubMed1997

Simple and rapid method for determining nicotinamide adenine dinucleotide synthetase activity by high-performance liquid chromatography.

A method is described for the determination of nicotinamide adenine dinucleotide synthetase (NADS) activity in human blood. Using high-performance liquid chromatography (HPLC), the formed NAD is separated from the substrates and the other blood components in less than 13 min. The activity of NADS determined by HPLC is closely correlated with that determined by the conventional spectrophotometric method, which requires two steps of enzyme reaction. The present method is simple and reliable and facilitates the routine analysis of NADS activity.

Adenosine Triphosphate↗
PubMed1997

Modulation of [3H]dopamine release by neuropeptide Y in rat striatal slices.

Neuropeptide Y, a 36-amino-acid peptide, has a wide and specific distribution in the central nervous system. In this study we examined the regulatory mechanisms of neuropeptide Y on dopamine release in the rat central nervous system. The effects of neuropeptide Y on the electrically stimulated [3H]dopamine release were investigated in superfused striatal slices of Sprague-Dawley rats, spontaneously hypertensive rats and Wistar-Kyoto rats. Neuropeptide Y (1 x 10(-8) - 1 x 10(-7) mol/1) reduced the stimulation (1 Hz)-induced [3H]dopamine release by a comparable amount in Sprague-Dawley rats. The blockade of dopamine D2 receptors by the dopamine D2 receptor antagonist, sulpiride, diminished the inhibitory effects of neuropeptide Y on the stimulation-evoked [3H]dopamine release. Pretreatment of slices with pertussis toxin (a potent inhibitor of G1-proteins) attenuated the suppression of the stimulation-evoked [3H]dopamine release by neuropeptide Y. Unlabelled dopamine itself reduced the stimulation-evoked [3H]dopamine release, and the inhibitory effect was also attenuated in the pertussis toxin-pretreated slices. In spontaneously hypertensive rats, the inhibitory effect of neuropeptide Y on the stimulation-evoked [3H]dopamine release was more pronounced than that in Wistar-Kyoto rats. The results of the present study showed that neuropeptide Y inhibited the stimulation-evoked dopamine release partially mediated by dopamine D2 receptors and the pertussis toxin-sensitive G1-proteins in rat striatum. Furthermore, the greater effect of neuropeptide Y on dopamine release in spontaneously hypertensive rats suggests a possible involvement of the peptide in regulating the central dopaminergic nerve activity in hypertension.

Animals↗
PubMed1997

Nicotinamide adenine dinucleotide synthetase activity in erythrocytes as a tool for the biological monitoring of lead exposure.

OBJECTIVE: The objective of this study was to evaluate the usefulness of nicotinamide adenine dinucleotide synthetase (NADS) activity for the biological monitoring of lead exposure. METHODS: The subjects were 76 male lead workers and 13 normal volunteers (7 males and 6 females). NADS activity and blood lead concentration (Pb-B) was determined in each subject. Delta-aminolevulinic acid dehydratase (ALAD) activity was determined in 58 lead workers out of 76 subjects. RESULTS: NADS activity in the lead workers ranged from 0.08 to 1.1 mumol/h per g of hemoglobin (gHb) and decreased linearly (r = -0.867) as Pb-B increased up to 81.6 micrograms/dl. The pattern of depressed activity of NADS was different from that of ALAD activity, which decreased rapidly and reached a plateau at the Pb-B level between 40 and 60 micrograms/dl. The Pb-B levels inducing 50% inhibition of the enzyme activities were calculated to be 43 micrograms/dl and 20 micrograms/dl for NADS and ALAD, respectively. At the Pb-B level of 40 micrograms/dl, NADS activity showed high validity (1.77) with predictivity of 0.92 at the cut-off level of 0.4 mumol/h per gHb, which were higher than those of ALAD activity. CONCLUSIONS: These results show an apparent dose-effect relationship of NADS activity versus Pb-B. NADS activity can be used for the biological monitoring of lead exposure.

Adult↗