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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 847 records · Page 47Linked to original sources
PubMed1987

Potassium secretion in the guinea pig distal colon.

Active K+ secretion in guinea pig distal colon was studied in vitro in Ussing chambers. Changes in short-circuit current (Isc), transepithelial conductance (Gt), and the unidirectional flux of 42K from serosa to mucosa (JKsm) were determined under a variety of physiological and pharmacological conditions. Mucosal tetraethylammonium (TEA) (10 or 30 mM) increased Isc, while it decreased Gt and JKsm. Seroal bumetanide (10(-4) M) also caused an increase in Isc and decreases in Gt and JKsm. The effects produced by TEA were abolished in the presence of bumetanide. The increase in Isc caused by bumetanide was greatly reduced by mucosal high-K+ conditions. Isoproterenol (10(-6) M), a beta-adrenergic agonist, elicited a decrease in Isc and an increase in Gt. Responses to isoproterenol (10(-6) M) were reduced or abolished by mucosal TEA, serosal bumetanide, serosal ouabain (10(-4) M), and serosal Na+- or Cl(-)-free conditions. Mucosal high K+ also reduced the isoproterenol-induced decrease in Isc. These results suggest that K+ secretion is electrogenic and dependent on the bumetanide-sensitive cotransport in the basolateral membrane. K+ exit across the apical membrane might be conductive and sensitive to TEA. In addition, beta-adrenergic agonists might stimulate K+ secretion.

Animals↗
PubMed1987

Role of renin-angiotensin and kallikrein-kinin systems on the mechanism of the hypotensive effects of converting enzyme inhibitor, alacepril.

In four patients with essential hypertension and one patient with renovascular hypertension, decreases in blood pressure and plasma angiotensin II levels, and increases in plasma renin activity and plasma kinin levels were observed during eight days of alacepril treatment. Significant correlations between the changes in mean arterial pressure and those in plasma angiotensin II or kinin levels were observed positively or negatively, respectively, in the essential hypertensives. These findings suggest that the hypotensive effect of alacepril might be caused mainly by a decrease in plasma angiotensin II levels and, at least in part, by an increase in plasma kinin levels.

Adult↗
PubMed1987

Minerals in plasma and urine and gustatory function tests for salt in a group of healthy young men.

Detection threshold for salt (NaCl) and discrimination between two levels of NaCl concentration (0.6 and 0.7%) in foods, and their relation to some selected biochemical parameters in plasma and urine (Zn, Na, K, Mg, Ca, Se for plasma and urine, Cu and retinol binding protein for plasma) were investigated in 15 healthy male college students. No subject failed to discriminate the NaCl concentrations in more than 50% of the tests. The rate of correct discrimination (RCD) was not associated with plasma Zn (P-Zn), plasma retinol binding protein (P-RBP), urinary potassium (U-K) or urinary sodium (U-Na), which significantly correlated with RCD in our previous study, while the detection threshold was significantly correlated with urinary Ca-Mg ratio (U-Ca/Mg), urinary Ca (U-Ca), U-Na, and urinary Mg. In the stepwise multiple regression analysis, U-Ca/Mg, plasma Ca, plasma Na, and RCD were selected as significant independent variables. These indicate that the status of minerals such as Na, Ca, and Mg is related to the gustatory function. One possible explanation for the discrepancy between the present and previous results is the elevated P-Zn and P-RBP levels in the present subjects.

Adult↗
PubMed1987

Interrelation between plasma kinin and the sympathetic nervous system in normal subjects.

To investigate the relationship between plasma kinin and the sympathetic nervous system, we measured plasma kinin, norepinephrine, and angiotensin-I-converting enzyme (ACE:kininase II) activity in normal subjects. In six normal subjects, subpressor and pressor doses of norepinephrine (10 ng/kg/min and 50 ng/kg/min, respectively) were infused for 1 hour. In five normal subjects, 60-degree head-up tilting was performed for 20 minutes. After norepinephrine infusion, plasma kinin levels were decreased significantly (p less than 0.01) with the subpressor dose of norepinephrine and were further decreased (p less than 0.01) with the pressor dose. Plasma ACE activity, however, showed no significant changes following these infusions. During the tilting, plasma kinin levels decreased significantly (p less than 0.01), whereas plasma norepinephrine levels increased significantly (p less than 0.01). From these results, the assumption of elevated levels in plasma endogenous or exogenous norepinephrine leads to a decrease in plasma kinin levels; this suggests that these two systems may be closely interrelated.

Adult↗
PubMed1987

The role of plasma angiotensin I converting enzyme in regulation of renin-angiotensin system activity in patients with essential hypertension.

In order to investigate the role of plasma angiotensin I (pAI) converting enzyme on the activity of the renin-angiotensin system, we measured plasma renin activity (PRA), plasma angiotensin II (pAII), and plasma angiotensin I converting enzyme (pACE) activity in fourteen patients with essential hypertension before and after two hours of ambulation combined with intravenous furosemide administration. Significant increases were observed in the values of PRA (p less than 0.005), pAII (p less than 0.005) and ACE activity (p less than 0.05) after ambulation. The ratios of log pAII/log PRA were increased significantly after ambulation (p less than 0.005), and a significantly positive correlation was observed between log pAII/log PRA and ACE activity (p less than 0.01). These results suggested that not only PRA but also ACE activity contributed to the activity of renin-angiotensin system through the generation of AII.

Adult↗
PubMed1986

Suppression of the hyperosmolarity response after cataract surgery.

The hyperosmolarity response was recorded with the electrooculogram in the dark before and after cataract extraction, to investigate a possible disorder in the retinal pigment epithelium after cataract extraction. The hyperosmolarity response was suppressed one week after surgery, especially after intracapsular extraction. The response recovered up to the preoperative level in most cases one or two months after surgery. These findings indicate reversible functional disorders of the pigment epithelium after cataract extraction, particularly intracapsular. This dysfunction can be revealed by the hyperosmolarity response. This response is clinically useful for diagnosis of pigment epitheliopathy after cataract extraction.

Adult↗
PubMed1986

A functional study of a case of glucagonoma exhibiting typical glucagonoma syndrome.

A 46-year-old man had a 7-year history of severe rash, which was then diagnosed as necrolytic migratory erythema. He had a weight loss of 6 kg, abnormal glucose tolerance test findings, anemia, glossitis, hair loss, and hypoproteinemia. Plasma amino acids levels were significantly decreased, and the fasting plasma glucagon (IRG) level was high at 5000 to 8000 pg/ml. Circulating IRG significantly increased after oral glucose loading, meal ingestion, and arginine infusion, and decreased with somatostatin infusion and insulin-induced hypoglycemia. No other gut or pancreatic hormone levels in plasma were elevated. Plasma IRG was eluted by gel-filtration, mainly in the position of true glucagon (MW 3500) by antiserum 30K. The rash was markedly improved after infusion of amino acids. Computerized tomography (CT) scan and celiac angiography revealed a large pancreatic tumor with multiple liver and lymph node metastases. The pancreatic tumor was totally resected, and was identified as glucagonoma by immunohistochemical technique. Since the plasma IRG levels remained high after surgery, the patient received dimethyltriazenoimidazole carboxamide therapy. After several courses of this treatment, plasma IRG levels decreased to 1000 to 2000 pg/ml, and the hepatic metastases were remarkably diminished in size.

Adenoma, Islet Cell↗
PubMed1986

Interrelation between the renin-angiotensin system and kallikrein-kinin system in patients with essential hypertension.

In order to investigate the relationship between the kallikrein-kinin (K-K) system and renin-angiotensin (R-A) system, plasma kinin (pKIN), plasma angiotensin II (pAII), plasma renin activity (PRA) and angiotensin converting enzyme activity (ACEA) were determined in 19 essential hypertensives (EHT). pKIN and pATII measurements were performed by highly sensitive radioimmunoassay (RIA), both of which were established in our laboratory. The assay sensitivity of pKIN and pAII were 0.5 pg/tube and 0.1 pg/tube, respectively. In pKIN RIA, pKIN was extracted by ethanol from 0.8 ml of plasma obtained with a syringe containing kinin generating and destroying enzyme inhibitors. In pAII RIA, pAII was measured directly in small amounts of 50-100 microliter, unextracted plasma samples. The level in pAII was significantly higher (p less than 0.05) in the normal renin group (NRH: n = 13) as compared with low renin group of EHT (LRH: n = 6). However, no significant difference was found in pKIN and ACEA between these two groups. Although a significantly positive correlation was observed between pAII and PRA (p less than 0.001) in EHT, the ratio of pAII/PRA tended to be higher in LHR than in NRH. ACEA correlated positively with pAII (p less than 0.01) or PRA (p less than 0.02), respectively. On the other hand, a significant negative correlation was also found between pKIN and pAII (p less than 0.05). From these findings, it was assumed that there was a closed relationship between R-A and K-K systems, and that angiotensin converting enzyme (kininase II) might play some role in the interrelation between both systems.

Adult↗
PubMed1986

The method of urinary total kallikrein and prekallikrein measurement, and their urinary excretions in the patients with essential hypertension.

The method of measurement for urinary total kallikrein (KAL) and preKAL in human was developed, and daily excretions of urinary total KAL, KAL and preKAL were investigated in patients with essential hypertension. Forty microliter of urine samples were incubated with or without 120 micrograms of chymotrypsin-free trypsin for total KAL or KAL, respectively. KAL was measured with direct radioimmunoassay and kininogenase assay. PreKAL was calculated by the subtraction of KAL from total KAL. The subjects of this study included 7 normotensives (NT) and 8 essential hypertensives (EHT). Daily excretions of total KAL, KAL and preKAL were significantly lower in EHT than those in NT. KAL/total KAL ratio, which reflects the conversion rate from preKAL to KAL in the kidney, was not significantly different between EHT and NT. From these results, it is suggested that decreased urinary KAL excretion in EHT is mainly caused by reduced preKAL production rather than the impaired conversion from preKAL to KAL in the kidney. It is emphasized that this method of measurement for urinary total KAL and preKAL may be a very useful tool for research of the renal kallikrein-kinin system.

Adult↗
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

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↗