Search PubMed⌕ Search

Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 37 records · Page 2Linked to original sources
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↗
PubMed2000

Walking 10,000 steps/day or more reduces blood pressure and sympathetic nerve activity in mild essential hypertension.

We investigated the effects of walking 10,000 steps/day or more on blood pressure and cardiac autonomic nerve activity in mild essential hypertensive patients. All subjects were males aged 47.0+/-1.0 (mean+/-SEM) years old. The original cohort consisted of 730 people in a manufacturing industry who measured the number of steps they walked each day using a pedometer. Eighty-three of these subjects walked 10,000 steps/day or more for 12 weeks. Thirty-two of these were hypertensives with systolic blood pressure (SBP) greater than 140 mmHg and/or diastolic blood pressure (DBP) greater than 90 mmHg. Thirty of these hypertensive subjects (HT) were examined twice, once during the pre- and once during the post-study period, for body mass index (BMI), maximal oxygen intake (Vo2max), blood pressure, heart rate (HR), and autonomic nerve activity by power spectral analysis of SBP and HR variability. In the HT group, walking 13,510+/-837 steps/day for 12 weeks lowered blood pressure (from 149.3+/-2.7/98.5+/-1.4 to 139.1+/-2.9/90.1+/-1.9 mmHg; p<0.01, respectively). In both the 34 normotensive controls and 17 hypertensive sedentary controls, blood pressure did not change. Walking also significantly lowered low-frequency fluctuations in SBP as an index of sympathetic nerve activity, from 1.324+/-0.192 to 0.738+/-0.154 mmHg2/Hz (p<0.05). VO2max rose significantly from 26.1+/-2.4 to 29.5+/-2.5 ml/kg/min (p<0.05). There were no changes in parasympathetic nerve activity, baroreceptor reflex sensitivity, or BMI. Our results indicate that walking 10,000 steps/days or more, irrespective of exercise intensity or duration, is effective in lowering blood pressure, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients.

Blood Pressure↗
PubMed2000

Diabetic ketoacidosis associated with Guillain-Barré syndrome with autonomic dysfunction.

A 37-year-old woman was admitted in a comatose state, after exhibiting fever and diarrhea. Diabetic ketoacidosis was diagnosed due to an increased blood glucose level (672 mg/dl), metabolic acidosis, and positive urinary ketone bodies. On the fifth hospital day, despite recovery from the critical state of ketoacidosis, the patient suffered from dysphagia, hypesthesia and motor weakness, followed by respiratory failure. Cerebrospinal fluid analysis was suggestive of Guillain-Barre syndrome (GBS). Autonomic dysfunction was manifested as tachycardia and mild hypertension in the acute stage. Marked orthostatic hypotension persisted long after paresis was improved, indicating an atypical clinical course of GBS.

Adult↗
PubMed2000

[Catecholamine].

Explore the source record for details and available documents.

Catecholamines↗
PubMed1999

Impaired endothelium-dependent relaxation in mesenteric arteries of reduced renal mass hypertensive rats.

Endothelium-dependent relaxation is not fully understood in volume-dependent models of hypertension. This study investigated the relaxation mediated by endothelium-derived nitric oxide (EDNO) and hyperpolarizing factor (EDHF) in superior mesenteric arteries from reduced renal mass hypertensive rats, an experimental model for volume-dependent hypertension. Hypertension was induced in male Wistar rats by subtotal nephrectomy and salt-loading (hypertensive group). The control group comprised rats that drank tap water after subtotal nephrectomy. Relaxation of isolated superior mesenteric arterial rings was investigated at the end of the 2-week study. In high K+-precontracted arterial rings, relaxation caused by acetylcholine (ACh) was markedly reduced in the hypertensive group compared with the findings for the control group (34+/-4% vs. 54+/-5% decrease in tension). In both groups, the relaxation was abolished by N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. In phenylephrine-precontracted arterial rings, relaxation caused by ACh was also small in the hypertensive group, while it was large in the control group (49 +/- 5% vs. 96 +/- 2%). Superfusion of L-NAME inhibited most of the relaxation caused by ACh, but the arteries still exhibited relaxation. Apamin, a blocker of Ca-dependent K+ channel, together with L-NAME further inhibited the residual relaxation. The relaxation inhibited by apamin was also reduced in the hypertensive group. We conclude that the relaxation inhibited by L-NAME was mediated by EDNO, while that inhibited by apamin was mediated by EDHF. Endothelium-independent relaxation caused by nitroprusside and diazoxide was normal in the hypertensive group. The relaxation mediated by both EDNO and EDHF was depressed in the arteries of reduced renal mass hypertensive rats as the result of an arterial endothelial abnormality.

Acetylcholine↗
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↗
PubMed1999

A new Ca-antagonist, azelnidipine, reduced blood pressure during exercise without augmentation of sympathetic nervous system in essential hypertension: a randomized, double-blind, placebo-controlled trial.

This study was carried out to evaluate the effect of a new long-acting calcium-channel antagonist, azelnidipine, on hemodynamic and neural responses to exercise. Ten patients (age, 36-69 years) with mild essential hypertension were enrolled in this study. A randomized, double-blind, crossover treatment of azelnidipine at a dose of 8.0 mg once daily for 4 weeks was performed. After a 4-week placebo period, the patients exercised in a submaximal test by using an ergometer with azelnidipine or placebo treatment. The changes caused by exercise in arterial blood pressure (BP), heart rate, cardiac output (CO), and systemic vascular resistance were evaluated. In addition, the plasma norepinephrine (NE), epinephrine (E), plasma renin activity, and plasma aldosterone concentration were determined at rest, at peak exercise, and at the recovery period. Both the SBP and diastolic (D) BP were decreased at rest by azelnidipine treatment (from 158 +/- 10/97 +/- 7 to 145 +/- 14/90 +/- 9 mm Hg). Azelnidipine significantly decreased both SBP and DBP during exercise (SBP, F = 6.09, p < 0.05, Fi = 0.612, NS; DBP, F = 17.78, p < 0.001, Fi = 0.298, NS). No significant changes in the resting heart rate and CO were observed, and the exercise-induced increase of these parameters was also not affected by azelnidipine. Azelnidipine produced no significant change of the resting plasma NE and E levels and an exercise-induced increase of plasma NE. In conclusion, these results indicate that azelnidipine, different from another dihydropyridine-type calcium channel antagonists, does not produce any changes in the hemodynamic and neurohumoral response to exercise, and it may be beneficial for patients with mild essential hypertension.

Adult↗
PubMed1999

Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.

Acute Disease↗
PubMed1999

Arterial relaxation mediated by endothelium-derived hyperpolarizing factor in hypertension induced by chronic inhibition of nitric oxide synthesis.

The aim of this study was to evaluate arterial relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) during chronic inhibition of nitric oxide (NO) synthase. We measured the isometric tension of isolated mesenteric arteries of Wistar rats administered Nomega-nitro-L-arginine methyl ester (L-NAME, 100 mg/Kg/day) for 3 weeks. Relaxation to acetylcholine (ACh) was reduced in L-NAME treated rats (maximum relaxation, 52% versus 79% ). After acute superfusion of 1x10(-4) M L-NAME, half the relaxation was inhibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treated rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDHF, reduced the relaxation. The relaxation inhibited by apamin was not significantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic deficiency of relaxation influence of NO.

Acetylcholine↗
PubMed1998

Enhanced efficacy of nilvadipine in hypertensives whose raised ambulatory blood pressure is sustained during sleep.

This study was designed to clarify the relationship between the antihypertensive effects of the calcium antagonist nilvadipine, and circadian changes in blood pressure. Based on measurements using an ambulatory blood pressure monitoring system (ABPM), 17 outpatients with untreated essential hypertension were divided into two groups: a sustained hypertensive group (with a fall in blood pressure during sleep < 10%, n = 7) and a waking time hypertensive group (with a fall in blood pressure during sleep > or = 10%, n = 10). During treatment with nilvadipine (8 mg/day, > or = 2 weeks), patients were reexamined by ABPM. The antihypertensive effect of nilvadipine was significantly and negatively correlated with the night time fall in blood pressure: this effect was significantly greater in the sustained hypertensive group than in the waking time hypertensive group. These data suggest that the long acting calcium antagonist nilvadipine has more potent antihypertensive effects in patients with sustained hypertension ("nondippers") than in those whose hypertension lessens during sleep ("dippers").

Aged↗
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

Anticoagulants in Takayasu's arteritis associated with crescentic glomerulonephritis and nephrotic syndrome: a case report.

The authors describe a 46-year-old Japanese woman who had Takayasu's arteritis associated with nephrotic syndrome due to mesangial proliferative glomerulonephritis with crescent. Although a few cases of focal and segmental mesangial proliferative glomerulonephritis associated with Takayasu's arteritis have been reported, nephrotic syndrome has not been reported previously in this situation.

Anti-Inflammatory Agents↗
PubMed1998

A premenopausal woman presenting with acute myocardial infarction of three different coronary vessels within 1 year: role of lipoprotein(a).

A premenopausal female patient presented with acute myocardial infarction of 3 different coronary vessels at different times within 1 year. These events were caused not by restenotic lesions after balloon angioplasty but by new lesions, which were successfully treated by primary angioplasty. Although she had a history of hypertension, type IIB hyperlipidemia, and diabetes, they had been well-controlled on medication. An elevated serum lipoprotein(a) level may have played a role in this rapid angiographic progression.

Angioplasty, Balloon↗