Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Makito Sato is active.

Publication


Featured researches published by Makito Sato.


Journal of the American Geriatrics Society | 1994

The Predictive Power of Self-Rated Health, Activities of Daily Living, and Ambulatory Activity for Cause-Specific Mortality among the Elderly: A Three-year Follow-up in Urban Japan

Ichiro Tsuji; Yuko Minami; Penelope M. Keyl; Shigeru Hisamichi; Hirotake Asano; Makito Sato; Kazuo Shinoda

Objective: To examine the predictive power of self‐rated health, activities of daily living (ADL), and ambulatory activity for different causes of death in a representative sample of older persons.


Journal of Hypertension | 1986

Effects of ouabain on blood pressure regulation in rats

Minoru Yasujima; Keishi Abe; Masaya Tanno; Masahiro Kohzuki; Yutaka Kasai; Makito Sato; Ken Omata; Kazuhisa Takeuchi; Kaoru Yoshinaga; Fuminori Masugi; Toshio Ogihara

In order to test the hypothesis that a circulating inhibitor of the sodium-potassium ATPase pump may cause a concomitant rise in blood pressure and increased sodium excretion, we studied chronic effects of continuous infusion of ouabain, an inhibitor of sodium-potassium ATPase, for up to 6 days on systolic blood pressure and urinary sodium excretion in conscious rats. We also evaluated the effect of this substance in rats with hypertension induced by chronic infusion of norepinephrine. Continuous infusion of ouabain (1.2 mg/kg per day) into the jugular vein by an osmotic minipump did not induce any changes in systolic blood pressure and urinary sodium excretion in intact rats on regular diets. Furthermore it did not cause a change in systolic blood pressure in rats drinking 1% NaCl, and in unilaterally nephrectomized rats drinking 1% NaCl, when compared with vehicle-infused animals. When the same dose of ouabain was administered simultaneously with 1.8 mg/kg per day norepinephrine infused intraperitoneally by another osmotic minipump in conscious rats, systolic blood pressure rose on day 1 to only 129.3 +/- 2.8 mmHg compared with the rist to 145.0 +/- 2.0 mmHg when norepinephrine alone was infused (P less than 0.01). The antihypertensive effect of ouabain was sustained for the entire experimental period lasting for 6 days and was not associated with any changes in urinary sodium excretion. The administration of ouabain to rats made hypertensive by a 3-day infusion of norepinephrine, returned the blood pressure to control levels, and the antihypertensive effect was sustained throughout the experimental period lasting a further 3 days and was not associated with any changes in urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)


Prostaglandins, Leukotrienes and Medicine | 1984

Sex and age-related differences in the urinary excretion of TXB2 in normal human subjects: a possible pathophysiological role of TXA2 in the aged kidney

Satoru Chiba; Keishi Abe; Kei Kudo; Ken Omata; Minoru Yasujima; Ko Sato; Masahide Seino; Yutaka Imai; Makito Sato; Kaoru Yoshinaga

Urinary excretion of thromboxane B2 (TXB2), a stable metabolite of TXA2, was measured by radioimmunoassay in 58 normal subjects (17 males and 41 females) aged from 19 to 98 years. The basal level of urinary TXB2 in normal subjects was 100 +/- 6.7 ng/day (mean +/- SEM). In young males, contamination of urine specimens with seminal fluid, which is known to contain large amounts of prostaglandin E, did not change the level of urinary TXB2. Urinary excretion of TXB2 was significantly higher in male subjects than in female (124 +/- 12.6 vs 90 +/- 7.4 ng/day, p less than 0.05). There was no significant age-related difference in 24-h urinary excretion of TXB2 in normal subjects. However, when urinary excretion of TXB2 was expressed as a function of urinary creatinine excretion, it was significantly higher in the elderly (60-93 years old) than in the younger subjects (19-59 years old)(141 +/- 15.7 vs 99 +/- 7.7 ng/g creatinine, p less than 0.02). Renal TXA2 may have a pathophysiological role in the functional impairment of the kidney in elderly people.


Gerontology | 1997

Dementia-free life expectancy among elderly Japanese

Catherine Sauvaget; Ichiro Tsuji; Yuko Minami; Akira Fukao; Shigeru Hisamichi; Hirotake Asano; Makito Sato

A 3-year prospective cohort study was conducted to estimate the life expectancy free of dementia (dementia-free life expectancy) in a representative sample of older persons living in an urban Japanese community. For the persons aged 65 years and older, who were not demented at the baseline survey in 1988, mortality and incidence rates of dementia were calculated. At the age of 65 years, males showed a total life expectancy of 18 years, including 16 years free of dementia, and females showed a total life expectancy of 23 years, including 18 years without dementia. At 65 years, the dementia-free life expectancy represented 89% of the total life expectancy for males and 79% for females. Total life expectancy and dementia-free life expectancy were longer among females than among males. However, the life-years with dementia were longer among females. This result would be attributable to a higher incidence of dementia and a lower mortality among females.


Journal of Hypertension | 1986

Effects of sodium and angiotensin II on urinary active and inactive kallikrein in rats

Minoru Yasujima; Keishi Abe; Masaya Tanno; Masahiro Kohzuki; Ken Omata; Yutaka Kasai; Kei Kudo; Kazuo Tsunoda; Makito Sato; Satoru Chiba; Kaoru Yoshinaga

To assess possible relationships between sodium balance, angiotensin II (ANG II), and renal active and inactive kallikrein, we studied the effects of sodium loading with 1% NaCl and chronic ANG II infusion (900 micrograms/kg per day) on the urinary excretion of total and active kallikrein for 6 days in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Sodium loading produced a sustained increase in urinary total, active and inactive kallikrein excretion. Chronic infusion of ANG II induced a sustained increase in urinary total, active and inactive kallikrein excretion in rats on a regular diet. In rats loaded with sodium, however, ANG II did not induce any further changes in urinary kallikrein excretion. Thus, the present study suggests that both sodium loading and ANG II infusion might stimulate the synthesis of renal kallikrein. In addition, it is suggested that ANG II infusion might stimulate the synthesis of kallikrein, at least partly, via the same mechanism as sodium loading does.


International Journal of Social Psychiatry | 1995

Physical Status and Dementia Risk: a Three-Year Prospective Study in Urban Japan

Yuko Minami; Ichiro Tsuji; Akira Fukao; Shigeru Hisamichi; Hirotake Asano; Makito Sato; Kazuo Shinoda

A three-year prospective study of 3,180 non-dementia persons in Sendai City, Japan was conducted to examine the effects of physical status and diseases diagnosed on dementia incidence. This cohort had been made at the initial survey in 1988 and the evaluation for incident dementia was performed on 2,461 respondents (77.4%) in a follow-up survey in 1991. Regarding physical status, the logistic regression including sex, age, health status, ambulatory activity and activities of daily living indicated that the poor health status and the limitation of ambulatory activity were significantly associated with an increased risk of dementia. The significant positive association with dementia was observed on stroke, respiratory disease and depression. This study identified the high risk population for dementia in the aspect of physical status.


American Heart Journal | 1982

Evaluation of the chronotropic property of captopril in hypertensive patients

Yutaka Imai; Keishi Abe; Makito Sato; Toshiaki Haruyama; Masao Hiwatari; Toshikazu Goto; Ko Sato; Yutaka Kasai; Jiro Tajima; Kaoru Yoshinaga

Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or beta-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decreases in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p less than 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captopril.U


Prostaglandins, Leukotrienes and Medicine | 1986

Urinary excretion of TXB2 after angiotensin converting enzyme inhibition in hypertensive patients

Kei Kudo; Keishi Abe; Satoru Chiba; Ken Omata; Ko Sato; Minoru Yasugima; Makito Sato; Kaoru Yoshinaga

Urinary excretion of thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2), was measured by radioimmunoassay in 7 essential hypertensive patients before and after a converting enzyme inhibitor, SQ 14225, administration. When a single oral dose of SQ 14225 (50mg) was given to 7 patients with essential hypertension, urinary excretion of TXB2 was increased significantly (from 58.9 +/- 18.1 to 116.1 +/- 20.7 pg/min, mean +/- SE, P less than 0.02) with simultaneous increase in plasma renin activity, urine volume, urinary sodium, urinary potassium and urinary excretion of PGE (from 58.8 +/- 12.8 to 135.1 +/- 30.0 pg/min, mean +/- SE, P less than 0.05). These results indicate that SQ 14225 stimulates vasoconstricting TXA2 production as well as vasodilating PGE production.


Prostaglandins, Leukotrienes and Medicine | 1982

Effect of dietary sodium intake on the metabolism of prostaglandins in the kidney in hypertensive patients

Makito Sato; Keishi Abe; Toshiaki Haruyama; Minoru Yasujima; Ko Sato; Satoru Chiba; Yutaka Imai; Masao Hiwatari; Yutaka Kasai; Jiro Tajima; Sadayoshi Itoh; Masahide Seino; Toshikazu Goto; Kaoru Yoshinaga

To investigate the role of renal prostaglandins (PGs) in the renal handling of sodium, urinary excretion of PGE, PGF2 alpha and PGF2 alpha MUM (main urinary metabolite of PGF2 alpha) were measured after various manipulations of dietary sodium intake in 8 hypertensive patients. A low sodium intake increased urinary excretion of PGF2 alpha MUM (p less than 0.05), but failed to change urinary excretion of PGE and PGF2 alpha. In contrast, a high sodium intake increased urinary excretion of PGE (p less than 0.01) and decreased urinary excretion of PGF2 alpha MUM (p less than 0.02). A low sodium intake decreased the ratio of urinary PGE/PGF2 alpha MUM and high sodium increased it (both p less than 0.001). There was a significant positive correlation between urinary excretion of sodium and that of PGE (p less than 0.001). Additional oral administration of potassium chloride did not change urinary excretion of PGs. These results may suggest that dietary sodium intake may be one of the regulators of the metabolism of PGs in the kidney, supporting the hypothesis that renal PGE has a natriuretic action in humans.


Prostaglandins and Medicine | 1980

Effect of propranolol on the urinary excretion of prostaglandin E and plasma benin activity in hypertensive patients

Makito Sato; Keishi Abe; Minoru Yasujima; Yoichi Otsuka; Satoru Chiba; Toshiaki Haruyama; Ko Sato; Yutaka Imai; Yutaka Sakurai; Toru Ito; Ken Omata; Kaoru Yoshinaga

To investigate the role of the renin-angiotensin (R-A) system in the release of renal prostaglandin E (PGE), urinary excretion of PGE, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured before and after the manipulation of the R-A system in hypertensive patients. After 7 days of the control sodium diet, the R-A system was stimulated by a combination of low sodium diet and oral administration of furosemide for 7 days. From the 4th day of sodium restriction, 40 mg/day of propranolol was administered per os for 2 days, and the dose was doubled for the following 2 days. PRA and PAC were significantly increased after the sodium restriction, but no change in urinary excretion of PGE was observed. Additional administration of propranolol for the following 4 days suppressed PRA significantly and PAC moderately, but it also failed to change urinary excretion of PGE. These results may suggest that renal medullary PGE synthesis, as reflected in urinary excretion of PGE, is not strongly dependent on the R-A system in these hypertensive patients.

Collaboration


Dive into the Makito Sato's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge