G Nomura

Kurume University, Куруме, Fukuoka, Japan

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Publications (19)47.18 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: In hypertensive subjects, exercise training is a therapeutic modality that not only lowers blood pressure but also corrects metabolic abnormality, such as hyperinsulinemia. Insulin causes sympatho-excitation via the modification of baroreflex, norepinephrine release, or central sympathetic outflow. However, the link between neural and metabolic changes by exercise training in hypertensive patients remains unknown. The aim of this study was to examine whether or not the blood pressure lowering effect of exercise training is associated with the improvement of insulin sensitivity in conjunction with the inhibition of sympathetic tone in hypertensive patients. We evaluated plasma insulin levels, arterial baroreflex function and humoral parameters before and after exercise training. Twenty-nine patients with essential hypertension under hospitalization participated in the study. Before and after three weeks of exercise training (75% max VO2, 6 min, q.i.d.), 24-hour blood pressure recordings, arterial baroreflex function testing and 75 g glucose tolerance tests were conducted. Area under the curve of insulin (sigma insulin) to glucose load was calculated as an index of hyperinsulinemia. Three weeks of exercise training decreased the 24-hour mean arterial pressure, heart rate and sigma insulin, and improved barorefiex function. There was a significant correlation between the reduction of arterial pressure and the change in sigma insulin. Furthermore, the reduction of sigma insulin was correlated with the improvement of baroreflex function and with the decrease in heart rate. Exercise training lowered the arterial pressure, with parallel changes in heart rate, baroreflex function and insulin resistance. The correction of sympathetic overactivity was closely associated with the amelioration of hyperinsulinemia. Our results suggest that the improvement of neuro-metabolic factors may be involved in the depressor effect caused by exercise training.
    Internal Medicine 01/2001; 39(12):1013-9. DOI:10.2169/internalmedicine.39.1013 · 0.90 Impact Factor
  • K Kohno · H Matsuoka · K Takenaka · Y Miyake · G Nomura · T Imaizumi ·
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    ABSTRACT: To clarify characteristics of the patients in whom exercise training lowers blood pressure and to elucidate the mechanisms by which exercise training lowers blood pressure, we evaluated 24-h blood pressure, glomerular filtration rate (GFR), renal blood flow (RBF), filtration fraction (FF), plasma renin activity (PRA), plasma aldosterone concentration (PAC), plasma norepinephrine concentration (PNE), and incremental area of insulin/glucose (sigmaI/sigmaG) during 75 g oral glucose tolerance test, and assessed arterial baroreceptor function (BSI) before and after a 3-week exercise training program (four 6-min sessions daily at 75% VO2 max). Patients were classified as responders (n = 15) if they showed statistically significant reduction in the multiple comparison of 24-h mean arterial pressure (MAP), or as nonresponders (n = 15) if they did not. Although there were no significant differences between responders and nonresponders in age, weight, MAP, GFR, RBF, RPF, FF, PNE, sigmaI/sigmaG, or BSI before exercise, renal vascular resistance (RVR; P < .05), PRA (P < .05), and PAC (P < .05) were significantly higher in responders than in nonresponders. The fractional excretion of sodium (FENa) (P < .05) were significantly lower in responders than in nonresponders. After exercise training, FF (P < .01), RVR (P < .05), PNE (P < .05) PRA (P < .01), and sigmaI/sigmaG (P < .05) decreased significantly only in responders. The decrease in MAP significantly correlated with the reductions in FF (r = 0.46, P < .05), PNE (r = 0.52, P < .01) and RVR (r = 0.40, P < .05). Thus, in patients who have higher RVR and PRA, exercise training lowered blood pressure in parallel to a reduction in RVR associated with decreases in sympathetic tone and improvement of insulin resistance. Our results suggest that exercise-induced changes in renal hemodynamics may contribute to the reduction in blood pressure in these patients.
    American Journal of Hypertension 08/1997; 10(8):859-68. DOI:10.1016/S0895-7061(97)00109-X · 2.85 Impact Factor
  • M Ninomiya · Y Ito · A Nishi · T Matsumoto · A Koga · Y Hori · H Nishida · G Nomura · H Kato ·
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    ABSTRACT: We describe a male patient with four episodes of acute renal failure after strenuous exercise occurring between the age of 14 and 25 years. He was found to have low serum uric acid (0.4 mg dl-1 after recovery) and high fractional excretion of uric acid. A benzbromarone/pyrazinamide test suggested that renal hypouricemia was due to defective proximal tubular reabsorption of uric acid at a presecretory site. A renal biopsy revealed acute tubular necrosis, a renal computer tomography scan showed patchy contrast enhancement and a treadmill exercise test induced an immediate fall in creatinine clearance. These findings suggest that the cause of acute renal failure was renal vasoconstriction rather than obstruction by uric acid crystals.
    Acta Paediatrica 09/1996; 85(8):1009-11. DOI:10.1111/j.1651-2227.1996.tb14206.x · 1.67 Impact Factor
  • M Tsuruta · R Hashimoto · H Adachi · T Imaizumi · G Nomura ·
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    ABSTRACT: To examine the hypothesis that hyperinsulinaemia is associated with the development of borderline hypertension or hypertension. Blood pressure status in non-obese normotensives (< 140/90 mmHg, n = 135) people were re-examined after 11 years after the baseline examination. Participants were selected from a 1981 population-based health examination and had a high blood glucose level or more than a trace of glucose in their urine. Out of 319 people recruited for further examination of glucose tolerance status, 135 normotensive participants with body mass index < 26 kg/m2 and without diabetes according to World Health Organization criteria were re-examined at the follow-up survey. Sixty-two (46%) out of 135 normotensive participants were hypertensive (defined as blood pressure > or = 140/90 mmHg) or receiving antihypertensive medication (n = 8) at the follow-up survey. Significant associations between the development of hypertension and baseline parameters were observed for systolic and diastolic blood pressure, serum triglycerides, high-density lipoprotein (HDL)-cholesterol, fasting and 60 min post-load insulin levels, and the sum of insulin concentrations from fasting to 180 min after glucose challenge after adjustments for age and sex. Odds ratios (95% confidence intervals) for the future development of hypertension between the highest and the lowest tertiles of insulin levels were 4.06 (1.40-11.76) for fasting insulin, 4.25 (1.45-12.45) for 60 min post-glucose load insulin, and 3.88 (1.34-11.20) for the sum of insulin concentrations, after adjustment for age, sex, systolic blood pressure, body mass index and alcohol consumption. Further adjustments for serum triglycerides and serum creatinine did not affect the insulin-hypertension relationship. The present study suggests that hyperinsulinemia is significantly related to the development of hypertension in non-obese and non-diabetic Japanese people.
    Journal of Hypertension 04/1996; 14(4):483-8. DOI:10.1097/00004872-199604000-00011 · 4.72 Impact Factor
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    ABSTRACT: Nitric oxide (NO) inhibits platelet adhesion and aggregation in vitro. In vivo, chronic inhibition of NO synthesis induces nephrosclerosis and hypertension. Although the pathophysiological mechanism of this glomerular injury has not been clarified, sympathetic nerve activation, a potent procoagulant stimulus elicited by NO inhibition, may play a role. To investigate the role of renal sympathetic nerves in the development of renal injury induced by NG-nitro-L-arginine methyl ester (L-NAME), a specific NO synthesis inhibitor, we examined renal histological changes in four groups of Sprague-Dawley rats: (1) sham operated, vehicle treated; (2) sham operated, L-NAME treated; (3) denervated, vehicle treated, and (4) denervated, L-NAME treated. Following renal denervation or sham operation, L-NAME was administered orally for 4 weeks. Chronic NO inhibition induced platelet aggregation and erythrocyte stasis in the glomerular capillary lumen accompanied by electron-microscopic glomerular injury. Renal denervation abrogated platelet aggregation and glomerular injury in L-NAME-treated animals. Thus, chronic NO synthesis inhibition induced intraglomerular platelet aggregation and glomerular injury, which was attenuated by renal nerve denervation. These results suggest that intrinsic NO may have an antithrombotic effect in the glomeruli and may play a protective role in the progression of glomerular injury possibly mediated by renal sympathetic nerves.
    Nephron 02/1996; 73(1):34-40. DOI:10.1159/000188995 · 13.26 Impact Factor
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    ABSTRACT: Nitric oxide inhibits proliferation and migration of vascular smooth muscle cells and contractility of cardiomyocytes in vitro. In spontaneously hypertensive rats (SHR), evidence suggests intrinsic abnormalities of the L-arginine-nitric oxide axis, such as low cGMP-dependent protein kinase in the heart and abnormal L-arginine metabolism. To investigate the in vivo effect of L-arginine on cardiac hypertrophy, 30 SHR and 30 Wistar-Kyoto rats (WKY) were randomly grouped to receive L-arginine (7.5 g/L in drinking water) or vehicle for 12 weeks. L-Arginine treatment did not affect body weight or arterial pressure in either strain. In vehicle-treated animals, the heart/body weight ratio was significantly higher in SHR than in WKY (P < .01). L-Arginine treatment decreased the heart/body weight ratio in SHR (P < .05) but did not affect it in WKY. Expression of skeletal alpha-actin mRNA, known to be expressed in the hypertrophied myocardium, was attenuated in L-arginine-treated SHR compared with vehicle-treated SHR. Cardiac cGMP content and nitrate/nitrite content were less in SHR than WKY. L-Arginine treatment increased these levels only in SHR, suggesting enhanced nitric oxide production. Thus, chronic L-arginine administration attenuated cardiac hypertrophy independently of blood pressure and increased myocardial content of cGMP and nitrate/nitrite. Our results suggest that abnormality of the cardiac L-arginine-nitric oxide axis may play an important role in the pathogenesis of cardiac hypertrophy in SHR.
    Hypertension 01/1996; 27(1):14-8. DOI:10.1161/01.HYP.27.1.14 · 6.48 Impact Factor
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    ABSTRACT: A 42-year old woman with hyperparathyroidism had a CT scan that was suggestive of a small nodular lesion in the left lower neck. Tc-99m sestamibi and Tc-99m tetrofosmin parathyroid imaging were performed 10 minutes and 2 hours after tracer injection. Early imaging with Tc-99m sestamibi demonstrated thyroid and focal uptake in the left lower neck. On delayed imaging, findings suggested a parathyroid adenoma. Imaging with Tc-99m tetrofosmin demonstrated similar findings. The abnormal parathyroid gland was an adenoma.
    Clinical Nuclear Medicine 11/1995; 20(10):902-5. DOI:10.1097/00003072-199510000-00010 · 3.93 Impact Factor
  • R Hashimoto · H Adachi · H Nishida · M Tsuruta · G Nomura ·
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    ABSTRACT: We conducted a prospective study in residents of a small farming community in southwestern Japan to determine whether elevated serum N-acetyl-beta-D-glucosaminidase (NAG) activity would predict future hypertension. The 505 normotensive subjects (blood pressure, < 140/90 mm Hg; mean age, 52 +/- 12 years) were reexamined after 7 years; 111 (22%) had become hypertensive (defined as blood pressure > or = 140/90 mm Hg and/or taking antihypertensive medication at follow-up). After adjustment for age and sex, the development of hypertension was significantly related to body mass index (P < .002), the sum of skinfolds (P < .001), baseline blood pressure (P < .0001), serum cholesterol (P < .01), serum uric acid level (P < .0001), and serum NAG activity (P < .005). Elevated NAG activity showed an independent relationship to future hypertension (P < .005) after adjustments for age, sex, baseline blood pressure (systolic, diastolic, or mean), uric acid level, and the sum of skinfolds. Therefore, elevated serum NAG activity was an effective indicator of future hypertension, and it might therefore be related to functional and/or structural changes in the cardiovascular system.
    Hypertension 06/1995; 25(6):1311-4. DOI:10.1161/01.HYP.25.6.1311 · 6.48 Impact Factor

  • Nihon Toseki Igakkai Zasshi 01/1995; 28(1):65-68. DOI:10.4009/jsdt.28.65
  • Source
    H Matsuoka · H Nishida · G Nomura · B N Van Vliet · H Toshima ·
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    ABSTRACT: Recent studies have indicated that chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, produces marked hypertension. Although the mechanism of this form of hypertension is not well understood, several studies have demonstrated that sympathetic nerve activity is at least acutely elevated after L-NAME administration. To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. After renal denervation or sham surgery, L-NAME was added to the drinking water (70 mg/100 mL) for 4 weeks, and arterial pressure was measured weekly by the tail-cuff method. L-NAME treatment caused a progressive increase in arterial pressure in sham-operated rats, rising to 154 +/- 6 mm Hg by week 4 of treatment compared with 115 +/- 2 mm Hg in the vehicle-treated sham-operated group (P < .005). In contrast, the development of hypertension was significantly delayed and attenuated in renal-denervated rats treated with L-NAME. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves.
    Hypertension 07/1994; 23(6 Pt 2):971-5. DOI:10.1161/01.HYP.23.6.971 · 6.48 Impact Factor
  • Y Hori · T Takamoto · H Nishida · T Ishizaki · M M Yokoyama · G Nomura ·
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    ABSTRACT: In order to clarify the abnormalities of cell-mediated immunity in patients with mesangial proliferative glomerulonephritis [IgA nephropathy (IgA N) and Non-IgA nephropathy (Non-IgA N)], lymphocyte subsets were analysed by using monoclonal antibodies with flow cytometric two-color analysis and interleukin-2 (IL-2) production from lymphocytes of the patients was measured by ELISA system. A markedly decreased percentage (11.6 +/- 10.5%) of CD4+ 45R+ cells was found in the patients with IgA N when the results were compared with the normal controls (20 +/- 6%) (P less than 0.01). No difference was found between patients with IgA N and the controls as to the percentage of CD4+ 45R-, CD8+, 11+ and CD8+ 11- cells, respectively. Patients with Non-IgA N also showed a significantly decreased percentage of CD4+ 45R+ cells (10.9 +/- 6.5%), while CD8+ 11+ cells was parallely lowered (7.4 +/- 5%) in compared with the controls (10 +/- 4%). The percentage of HLA-DR positive cells was found to be increased in the patients with both IgA N and Non-IgA N, although the antigen bearing cells were reduced after stimulation with Concanavalin-A (Con-A). No difference in IL-2 production from lymphocyte of both patients groups and the controls cultured with Con-A was found. These results suggested that a deficiency of suppressor inducer T cells played a part of the pathogenesis of IgA N and Non-IgA N.
    Nippon Jinzo Gakkai shi 08/1989; 31(7):723-33.
  • M Ueda · G Nomura · H Shibata · H Nishida · A Moriyama · E Kumagai · H Toshima ·
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    ABSTRACT: 1. To investigate whether cardiopulmonary baroreflex control contributes to the pathogenesis and progression of hypertension, we have evaluated the function of the cardiopulmonary baroreflex in 22 patients with essential hypertension and in 17 volunteers with normotension. The normotensive group consisted of 8 subjects with a family history of hypertension and nine with no family history. 2. Forearm vascular resistance (FVR) and central venous pressure (CVP) were measured under control conditions when -10 mmHg lower body negative pressure was applied; the cardiopulmonary slope (CPS = delta FVR/delta CVP) was calculated as an index of the cardiopulmonary baroreflex function. 3. CPS was significantly higher in hypertensives (6.0 +/- 3.93 [s.d.], P less than 0.01) and also tended to be higher in normotensives with a family history of hypertension (3.9 +/- 3.53, P less than 0.05), compared with normotensives without a family history of hypertension (1.7 +/- 0.88). 4. When the hypertensives were divided into two groups, depending on whether CPS was greater or less than 6.0 units, cardiac wall thickness (20 +/- 1.6 mm vs 23 +/- 3.2 mm, P less than 0.05) and the renal vascular resistance (20.9 +/- 6.52 units vs 28.9 +/- 7.32 units, P less than 0.05) were both significantly higher in the Low CPS group. 5. These findings suggest that cardiopulmonary baroreflex function was augmented even in normotensive subjects with hypertensive relatives, as compared with those without hypertensive subjects. Furthermore, cardiopulmonary baroreflex function was augmented in the early stages of hypertension and diminished further with increasing severity.
    Clinical and experimental pharmacology & physiology. Supplement 02/1989; 15:89-92.

  • Kokyu to junkan. Respiration & circulation 04/1988; 36(3):317-21.
  • H Shibata · G Nomura · A Moriyama · M Ueda · E Kumagai · H Toshima ·

    Kokyu to junkan. Respiration & circulation 04/1987; 35(3):283-9.
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    ABSTRACT: Serum N-acetyl-beta-D-glucosaminidase (NAG) levels were measured in 1080 residents in Tanushimaru, Fukuoka, aged 20 to 84 years old, during a periodical epidemiological survey performed in 1982. Thirteen pregnant women were excluded from this study. Serum NAG levels showed an increase with age, but were not different between sexes. We found high serum NAG values in those with high blood pressure, high serum total cholesterol, low serum HDL-cholesterol, or reduced creatinine clearance rate, and women with high serum uric acid, increased skinfold thickness, or high hematocrit. Multiple regression equation was as follows: NAG = 3.53 + 0.07 (age) + 0.14 (hematocrit) + 0.03 (total skinfold thickness) + 0.04 (systolic blood pressure) - 0.03 (HDL-cholesterol) - 0.04 (mean blood pressure) - 0.01 (creatinine clearance). The multiple correlation coefficient was 0.37 (F = 24.4). We suggest that NAG may be a useful index in screening cardiovascular impairment and for cardiovascular risk factors.
    Japanese Circulation Journal 02/1985; 49(1):68-74. DOI:10.1253/jcj.49.68
  • T Ishizaki · T Kitano · K Midorikawa · K Adachi · K Ohta · G Nomura · M Morimatsu ·

    Nippon Jinzo Gakkai shi 11/1984; 26(10):1329-36.
  • E Kumagai · G Nomura · K Midorikawa · Y Koga ·

    Kokyu to junkan. Respiration & circulation 02/1983; 31(1):63-6.

  • Nippon Jinzo Gakkai shi 11/1982; 24(10):1181-7.
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    ABSTRACT: We attempted to clarify the pathogenesis of asymmetric ventricular hypertrophy in hypertensive patients, especially regarding sympathetic nervous system and renin-angiotensin system. Subjects were divided in 3 groups by echocardiographic findings; 1) 15 patients with non-hypertrophy (NH), 2) 14 patients with symmetric hypertrophy (SH), and 3) 10 patients with asymmetric hypertrophy (ASH). Subjects with ASH showed following features. Age (53.7 +/- 1.6 yr) was older than NH (43.7 +/- 1.4 yr) but not different from SH (49.7 +/- 2.3 yr). Mean arterial pressure (119.0 +/- 3.9 mmHg) was higher than NH (107.5 +/- 1.4 mmHg) but not different from SH (122.4 +/- 2.8 mmHg). End-diastolic and end-systolic dimensions were smaller and ejection fraction was larger than those of NH and SH. Cardiac index (3.90 +/- 0.37 L/min/M2) was largest among 3 groups. UNE (19.5 +/- 2.5 micrograms/day) was lower than SH (31.2 +/- 2.5 micrograms/day). PRA (0.44 +/- 0.16 ng/ml/h) was lower than SH (1.53 +/- 0.20 ng/ml/h) and NH (1.62 +/- 0.28 ng/ml/h). Ejection fraction was correlated with UNE (r = 0.835) and PRA (r = 0.736). We suggest that the heart of hypertensives with ASH is in hyperdynamic state due to the hyperresponsiveness to sympathetic stimuli, although they have a decrease of sympathetic nervous activity, and the renin-volume axis may have no important role on the pathogenesis of ASH.
    Japanese Heart Journal 04/1982; 23(2):181-90. DOI:10.1536/ihj.23.181 · 0.40 Impact Factor

Publication Stats

258 Citations
47.18 Total Impact Points


  • 1982-1997
    • Kurume University
      • Department of Internal Medicine
      Куруме, Fukuoka, Japan
  • 1994
    • Memorial University of Newfoundland
      Saint John's, Newfoundland and Labrador, Canada