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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 127 records · Page 7Linked to original sources
PubMed1986

The role of renal kallikrein-kinin system and prostaglandins in diuresis and natriuresis following saline infusion in normotensives and essential hypertensives.

In order to clarify the significance of the renal kallikrein(KAL)-kinin(KIN) system and prostaglandins (PG) in exaggerated natriuresis in essential hypertensives, the effect of acute sodium load on urinary KAL, KIN, PG, and renal water and sodium handling were investigated in normotensives (NT) and patients with essential hypertension (EHT). Nine NT and seven EHT were studied following acute physiological saline infusion (1000 ml/2 hrs). Urine volume (UV), urinary sodium excretion (UNaV), fractional excretion of sodium (FENa), and fractional excretion of inorganic phosphorus (FEP) were measured by the clearance method. Urinary KAL and KIN were determined by direct-RIA. Urinary kininase (total, I and II) activities were measured by the kinin destroying capacity. Urinary PGE was measured by RIA. Following saline infusion, UV, UNaV, FEP, KAL, KIN and PGE significantly increased in both NT and EHT. The increases of UV, UNaV, FENa, FEP and KAL were remarkably greater in EHT than each in NT, while no significant difference was found in the increment of PGE between NT and EHT. Significantly positive correlations were observed between PGE and KAL or KIN in NT (r = 0.889, p less than 0.005; r = 0.574, p less than 0.05, respectively), but not in EHT. From these results, it was concluded that the exaggerated natriuresis observed in EHT following infusion may be significantly related to the augmentation of renal KAL-KIN system, but was not directly related to PGE.

Diuresis↗
PubMed1986

Comprehensive studies on the renal kallikrein-kinin system in essential hypertension.

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1986

A comparative study of the measurement of urinary kallikrein by various methods in patients with essential hypertension and patients with proteinuria.

In order to investigate the validity of urinary kallikrein (KAL) measurement, comparative studies were performed among the values obtained by various methods of urinary KAL measurements. Daily urine samples were collected from 37 hospitalized normal subjects (NS, 21 essential hypertensives without complications (EHT) and 20 patients with renal diseases associated with proteinuria (PU). Urinary KAL excretions were determined by direct radioimmunoassay (RIA), kininogenase assay (K-genase), TAMe esterase assay (TAMe), and PPA-MCA (MCA) and PPA-NE amidase assay (NE). By the desalting procedure, urinary KAL levels showed significant changes in TAMe, MCA and NE, but not in d-RIA and K-genase in all three groups. In TAMe, MCA and NE, the recovery of added KAL in urine was significantly lower in non-desalted samples in both EHT and PU, but not in NS. Impaired recovery and correlations between d-RIA or K-genase and TAMe, MCA or NE in non-desalted samples were improved by desalting. Although good correlations were observed between d-RIA or K-genase and TAMe, MCA or NE in desalted samples, the slopes of curves were steeper in EHT and PU than in NS, suggesting that the synthetic substrate methods still have some problems in the KAL measurement in these pathological states, KAL inhibitor, aprotinin and gabezate mesilate did not suppress the esterclytic and amidolytic activities completely, but suppressed K-genase activity completely in PU urine samples, suggesting that certain kinds of non-KAL esterases might remain in PU urine samples. Thus, d-RIA and K-genase appear to be the most reliable methods in the measurement of urinary KAL quantity and activity, respectively.

Humans↗
PubMed1986

Purification of human low molecular weight kininogen and its application for a simple ND sensitive method for determination of human urinary kallikrein activity.

Human plasma low molecular weight kininogen was purified with ammonium sulfate fractionation, DEAE-cellulose, CM-Sephadex C-50 and aprotinin-agarose affinity column chromatography, after which this was further purified with Sephadex G-150 and DEAE-Sephadex A-50 column chromatographies. Kallikrein activity was measured as the kininogenase activity reflecting the kinin-producing capacity from kininogen. The purification factor from crude plasma to purified substrate was 44-fold, and the recovery was 18%. The purified human substrate did not contain kinin-generating or destroying enzymes which would interfere with kininogenase activity, and showed a cross-reactivity of less than 0.1% against kinin antiserum. In the kininogenase assay, all kininogen was removed by adding ethanol to terminate the enzyme reaction. Because of the high sensitivity of kinin radioimmunoassay, the kinin levels in urine could be determined in very small amounts of samples (0.5 to 2.0 nl of the original urine). These findings indicated that kinin levels in incubation solution could be measured directly, and the control tubes are unnecessary in this assay procedure. In a comparison among human, dog and bovine low molecular weight kininogen as the substrate for human urinary kallikrein, the enzyme activity was 5 and 80 fold higher in the human low molecular weight kininogen, respectively, suggesting that a human substrate is the best for human enzymes. This simple, specific, sensitive and homologous kininogenase assay system seems to be very useful investigating the physiological or pathophysiological role of the renal kallikrein-kinin system in hypertensive and renal diseases.

Animals↗
PubMed1986

Clinical evaluation of bisoprolol in patients with hypertension: interim report.

The antihypertensive effect and possible adverse effects of bisoprolol were assessed in 96 Japanese patients with mild to moderate hypertension. After a 2- to 4-week placebo period, bisoprolol was administered to 68 outpatients at a daily dose of 5 mg to 20 mg for 6 to 8 weeks, and to 28 inpatients with the same dose range up to a maximum of 4 weeks. For outpatients, blood pressure and heart rate were recorded every 2 weeks, while for inpatients, in addition to daily measurements, the effect of bisoprolol on diurnal variation of blood pressure was also studied. Bisoprolol lowered blood pressure and heart rate significantly in both groups of patients. The most common adverse effect was bradycardia. It is expected that bisoprolol will be a very effective and useful antihypertensive drug.

Adrenergic beta-Antagonists↗
PubMed1986

A case of adrenal tumor producing renin, aldosterone, and sex steroid hormones.

A 27-year-old woman with an adrenal tumor that produced renin and aldosterone, associated with hypertension and adrenogenital syndrome, is described. Severe hypertension, cardiomegaly, a low serum potassium level, clinical symptoms of adrenogenital syndrome, and a left upper abdominal tumor also were found. Endocrinological studies showed that plasma and urinary levels of sex steroid hormones such as dehydroepiandrosterone, androsterone, and testosterone were markedly increased. Plasma renin activity, plasma angiotensin II, and plasma aldosterone levels also were increased markedly, although deoxycorticosterone levels remained within the normal range. The possibility of renovascular hypertension was excluded by angiography of the renal artery and by venous sampling of plasma renin activity. Abnormal elevations in plasma aldosterone levels persisted despite normalization of plasma angiotensin II by converting enzyme inhibitor administration. It was suspected that this patient had an adrenal tumor producing renin as well as sex steroids and aldosterone. Microscopy of the resected tumor revealed that the tumor was composed mostly of cells with large nuclei and light cytoplasm. The tumor contained dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, aldosterone, and renin. Immunohistochemical study showed that some of the tumor cells produced renin. Biopsy of the left renal tissue showed evident atrophy of the juxtaglomerular cells and pronounced arteriosclerosis. After resection of the tumor, all blood and urinary levels of the abnormally increased hormones returned to a normal range and an apparent fall of blood pressure was noted. To our knowledge, this is the first report of a renin and aldosterone-producing adrenal tumor associated with hypertension and adrenogenital syndrome.

Adrenal Gland Neoplasms↗
PubMed1986

Sympathetic nerve activity, plasma renin activity and water-sodium balance in obese patients with essential hypertension.

Studies were conducted to evaluate the role of water-sodium metabolism on the hypertensive mechanisms in obese patients with essential hypertension (EHT). The obesity index correlated positively with the mean arterial pressure, plasma volume, extracellular fluid volume or total exchangeable sodium, and negatively with plasma noradrenaline concentration or plasma renin activity in EHT. Hypotensive effects of sodium restriction (Na 35 mEq, K 75 mEq) or the natriuretic response to infused dopamine (3 micrograms/kg/min) was remarkable in obese EHT. Fractional excretion of sodium (FENa), which reflects the renal tubular reabsorption of sodium, was significantly lower in obese EHT than that in non-obese or mildly obese EHT. Urinary excretion of free dopamine (UDA) had a positive relationship with simultaneously measured urinary excretion of sodium or FENa. In addition, UDA correlated positively with the obesity index in patients whose weight was under 115% of the ideal weight. On the contrary, the relation between the two parameters was significantly negative in patients whose weight was over 115% of the ideal weight. These findings suggest that the expansion of body fluid volume and sodium, which might result from the blunted natriuretic ability, at least in part, due to an attenuation of the renal dopaminergic activity, play an important role of the hypertensive mechanisms in obese EHT.

Adult↗
PubMed1986

A case of lactate dehydrogenase (LDH)-IgG complex formation which causes low plasma LDH activity and an abnormal LDH isozyme pattern.

A case of an LDH-IgG complex formation which causes low plasma LDH activity and an abnormal LDH isozyme pattern was reported. A patient had pericarditis and myocardial hypertrophy of asymmetrical septal hypertrophy type. The same IgG was recognized in pericardial effusion. From a column chromatographic study, the molecular weight of LDH-IgG complex was estimated as being about 490,000. This complex was speculated as the IgG1-LDH2. The mechanism by which LDH-IgG is formed and the relationship between the complex itself and cardiac diseases remain unknown.

Aged↗
PubMed1986

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

In order to clarify the mechanism of the hypotensive action of captopril, the acute and chronic effects of this drug on the kallikrein-kinin and renin-angiotensin systems were investigated respectively in 14 and 19 patients with hypertension. To determine the acute effect, a dose of 50 mg of captopril was administered once orally. For the chronic effect, 75-300 mg of the drug was administered daily for 14 days. In observations of the acute effect, blood pressure decreased significantly at 30 min. and maximally at 60-180 min. after administration with no change in heart rate. Significant increases in blood kinin levels and plasma renin activity (PRA), and a decrease in plasma angiotensin II levels were also observed. A marked augmentation was also found in urinary kinin excretion, but not in urinary kallikrein excretion. Moreover, the changes in blood pressure significantly correlated negatively with basal PRA, basal plasma angiotensin II and the changes in blood kinin levels, and positively with the changes in plasma angiotensin II. In our study of the chronic effect of captopril, similar changes in blood kinin levels, PRA, plasma angiotensin II levels, blood pressure and heart rate to the acute effect study were observed. Significant correlations of the changes in blood pressure were found negatively with basal PRA, basal plasma angiotensin II levels and the changes in blood kinin levels and positively with the changes in plasma angiotensin II levels. In addition, significant increases in urine volume and urinary sodium excretion occurred following administration of captopril for 14 days, and both increases negatively correlated with the changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Localization of renal kallikrein-kinin system components in the kidney.

In a study using a stop-flow technique in dog kidney, the existence of kallikrein and kinin was recognized in distal tubules. The presence of kininase I was seen in both distal and proximal tubules, and also partly in the distal tubules. The presence of kininase II in the distal tubules was again confirmed by pretreatment with SQ14225. No evidence of kinin formation, however, was obtained in the proximal nephrons in stop-flow method. From these results, it was suggested that kininase I and II localized in proximal tubules may destroy the kinin filtered from glomeruli at the proximal level, while kallikrein and kininogen and also kininase I and II in the distal tubules may regulate the activity of the renal kallikrein-kinin system in the distal nephrons.

Animals↗
PubMed1986

[Qualitative determination of infarct segment by Fourier analysis using gated cardiac pool emission computed tomography].

As a new method for regional wall motion analysis, the tomographic functional images, including "coronal", "sagittal" and "four-chamber" sections, were produced by applying the fundamental Fourier analysis using gated cardiac pool emission computed tomography (POOL-SPECT). Segmental wall motion was qualitatively assessed from the functional images in 10 normal subjects and in 48 patients with myocardial infarction. The results were compared with those assessed by gated blood pool planar images (modified LAO 45), two-dimensional echocardiography (2DE) or contrast left ventriculography (LVG). The following results were obtained. 1. POOL-SPECT imaging could separate the ventricle in three dimensions from the neighboring cardiovascular system by avoiding the overlapping blood pool to make accurate recognition of regional wall motion. 2. The functional tomograms had greater clinical efficacy in the diagnosis of infarcted segments than did the conventional equilibrium method, with high sensitivity (93/99, 93.9%), specificity (128/141, 90.8%) and accuracy (221/240, 92.1%), especially in the apical and inferoposterior portions. 3. Tomographic functional imaging facilitated estimating segmental cardiac performance from spatial and temporal aspects. The amplitude image which expresses regional stroke volume was readily available to detect hypokinesis and akinesis. The phase image of the initial cardiac movement was very useful for diagnosing dyskinesis. 4. In comparing the qualitative analysis with 2DE or LVG, complete agreement was observed in 80% (128/160) and 85.1% (149/175) of segments, though POOL-SPECT imaging showed underestimations in 11% of the segments. In conclusion, POOL-SPECT can be performed repeatedly without potential risks and the tomographic functional images derived from application of Fourier analysis to POOL-SPECT images are very useful for qualitative and three-dimensional analysis of regional wall motion. Thus, this technique may be a promising procedure in clinical investigations, obviating the disadvantages of conventional methods.

Adult↗
PubMed1985

Plasma prolactin levels in patients with essential hypertension, malignant hypertension and secondary hypertension.

Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. From these results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences may partly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanism of plasma prolactin increment.

Adolescent↗
PubMed1985

The effect of blood volume changes accompanying isotonic circumstances on plasma antidiuretic hormone levels in normal subjects.

Changes in plasma ADH levels were investigated in human male subjects whose blood volume was altered under isotonic circumstances. Blood volume was reduced by ambulation and increased by isotonic saline infusion in an overnight dehydrated state, and determinations were made on plasma ADH levels, plasma osmolality and hematocrit values. Plasma ADH levels were clearly affected by the small changes in blood volume, and significantly negative correlation was found between plasma ADH levels and the percent changes in blood volume under isotonic circumstances. From these findings, it was concluded that ADH release in human subjects is also controlled by the changes of the blood volume factor in addition to osmotic stimuli.

Adolescent↗
PubMed1985

Urinary excretions of kininase I and kininase II activities in essential hypertension. A sensitive and simple method for its kinin-destroying capacity.

To further clarify the role of the renal kallikrein-kinin system in essential hypertension, a sensitive and simple method for the determination of both human urinary kininase I and kininase II was established, and the system components were determined in patients. In the measurement of kininase activity, desalted urine samples were incubated with synthetic bradykinin, and the reaction was terminated with kininase inhibitors, ethylene diamine tetraacetic acid and phenanthroline. Thus, kininase activity was determined as the kinin-destroying capacity. Moreover, the specific inhibitor for kininase II, SQ14225, was applied for the separation of kininase I and kininase II activities. Daily urinary excretions of total kininase and kininase I activities were significantly higher in essential hypertensive patients than those in normotensive subjects, whereas no difference was observed in kininase II activity. As reported previously, daily excretions of urinary kallikrein and kinin simultaneously determined in these patients were significantly lower than excretions in normotensive subjects. From these results, it was suggested that not only decreased renal kallikrein, but also increased kininase activity, may play an important role in the suppression of the renal kallikrein-kinin system through the reduction of active kinin level in essential hypertension.

Adolescent↗