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Biomedical subjects

K Shimamoto

Publications and source records attributed to K Shimamoto.

At least 397 records · Page 22Linked to original sources
PubMed1982

An improved method for the determination of human blood kinin levels by sensitive kinin radioimmunoassay.

A highly sensitive and specific radioimmunoassay for kinin (minimal detectable amount, 0.5 pg/tube) was applied to measure the blood kinin level. A five ml blood sample was collected with a siliconized needle and plastic syringe which contained 2.5 ml of 0.8 N-HCl. The blood kinin was extracted with butanol, following reextraction with water. According to this procedure, the mean recovery (mean +/- SE) calculated from added 125I-bradykinin (500 CPM) and the known amounts of cold bradykinin were 50.4 +/- 0.8% and 51.1 +/- 2.2%, respectively. In comparison with other sampling methods in 6 normal subjects, the blood samples taken without HCl in syringes showed a higher level (24.4 +/- 10.1 pg/ml) than the samples with HCl (5.3 +/- 1.3 pg/ml). And very high levels were obtained in the plasma samples collected by the method of Talamo or Vinci (0.53 +/- 0.24 ng/ml and 3.5 +/- 1.3 ng/ml, respectively). The kinin content in blood samples taken with HCl was stable at -20 degrees C for at least one month, but increased significantly at room temperature or 4 degrees C for 48 hours. Blood samples were obtained from 17 normal subjects, and 3 patients with acute myocardial infarction. Blood kinin levels in the patient with acute myocardial infarction, 121 +/- 20.9 pg/ml, were significantly higher than those in normal subjects (3.8 +/- 0.5 pg/ml). From these results, it was concluded that high levels of blood kinin reported previously may have resulted from inadequate sampling procedures. Thus, in order to measure blood kinin accurately, inactivation of the kinin generating and destroying enzymes must be done immediately after the sampling. In addition, this radioimmunoassay method should be very useful in investigating the pathophysiological role of blood kinin in various diseases.

Blood Specimen Collection↗
PubMed1982

A method for determination of human urinary inactive kallikrein (prekallikrein).

Inactive kallikrein (prekallikrein) in human urine was discovered recently. A more accurate method to measure this zymogen and total kallikrein is described. With trypsin pretreatment, it was found that 35.3 +/- 2.7% of total urinary kallikrein activity was prekallikrein. The results are supported by a new direct radioimmunoassay which measures predominantly active kallikrein.

Adult↗
PubMed1982

[Kallikrein].

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Animals↗
PubMed1981

Kallikrein-induced uterine contraction independent of kinin formation.

Responses of smooth muscle to kallikreins (EC 3.4.21.8) are generally considered to result from kinin formation. This premise was reexamined with the isolated rat uterus. Rat urinary kallikrein or bradykinin produced dose-dependent contractions of rat uterus but kallikrein was 5-fold more potent than bradykinin. Kallikrein caused an immediate series of rhythmic contractions which could be increased gradually with subsequent addition of kininogen substrate. Kallikrein-induced contractions were unaffected by carboxypeptidase B or a bradykinin antiserum whereas bradykinin-induced contractions were attenuated or abolished. Other serine proteinases, including trypsin, either did not induce contraction in the absence of added kininogen or did so minimally. Although small amounts of kininogen-like substrate were found in uterine tissue, detectable kinin levels (greater than 4 pg) could not be found in bathing media during maximal kallikrein-induced contractions or after uterine tissue was incubated with high concentrations of the enzyme in the presence of SQ 20881, a kininase II inhibitor. The data suggest that uterine contraction produced by a homologous kallikrein does not involve kinin formation but results from an action of this serine proteinase upon other accessible systems coupled to the contractile response.

Animals↗
PubMed1981

Movement of C-compounds from Maternal Tissue into Maize Seeds Grown in Vitro.

Uptake from nutrient media into the cob and translocation of various (14)C-compounds from maternal tissue (cob) into developing maize seeds was examined by using caryopsis cultures. Based on relative (14)C concentrations in the cob and the endosperm, it was concluded that the relative efficiencies of movement of amino acids (leucine, phenylalanine, proline), vitamins (thiamine HCl, nicotinic acid), and nucleic acid bases (adenine, thymine) from the cob to the endosperm were 11 to 250 times lower than that of sucrose. Thiamine was unique in that it was concentrated in the embryo at a level that was almost 10 times higher than in the endosperm. The absence of auxotrophic mutants requiring an organic supplement in higher plants (other than thiamine auxotrophs) may be explained by inadequate translocation of these essential metabolites into the mutant zygotes (embryos) to enable their development to mature seeds.

Journal Article↗
PubMed1981

Excretion of human urinary kallikrein quantity measured by a direct radioimmunoassay of human urinary kallikrein in patients with essential hypertension and secondary hypertensive diseases.

Recently, we established a very sensitive, specific and simple direct radioimmunoassay method for human urinary kallikrein. In this study, in order to clarify whether or not the low or high excretion rate of urinary kallikrein activity in patients with essential hypertension, primary aldosteronism, pheochromocytoma and Bartter's syndrome is caused by changes in enzyme quantity, urinary kallikrein excretion was measured with this direct radioimmunoassay method in normal subjects and in patients with these diseases. Urinary kallikrein excretion measured as enzyme quantity was significantly lower in patients with essential hypertension, and higher in patients with primary aldosteronism and Bartter's syndrome. These results are consistent with other previously reported data and our data measured by means of esterase assay or kininogenase assay. The results also suggest that lowered or elevated excretion of urinary kallikrein activity in these diseases is caused, in part at least, by the lowered or elevated excretion of enzyme quantity.

Bartter Syndrome↗
PubMed1980

The radioimmunoassay of human urinary kallikrein and comparisons with kallikrein activity measurements.

Human urinary kallikrein was purified to homogeneity, and an antiserum to it was raised in rabbits. A RIA was devised which uses this rabbit antiserum (Keq = 2.75 x 10(11) M-1) in a final dilution of 1:2,500,000 and the purified kallikrein labeled with 125I using a lactoperoxidase method. Assay sensitivity is 8 pg kallikrein. Thus far, the assay is specific for human and perhaps monkey urinary kallikrein. Correlations between this assay of immunoreactive kallikrein and the alpha-N-Tosyl-L-arginine-[3H]methylester (Tos-Arg-OMe) activity method or a kininogenase assay were highly significant (r = 0.94 and 0.96, respectively) and show that each assay measures human urinary kallikrein comparably. Low or high dietary sodium intakes, maneuvers known to change human urinary Tos-Arg-OMe esterase excretion, change immunoreactive kallikrein to an equivalent degree. Normal black children, already known to excrete significantly less Tos-Arg-OMe esterase than white children, excrete similarly reduced amounts of immunoreactive kallikrein. Kallikrein excretion in children with cystic fibrosis of the pancreas was not different from that in normal children. The data show that a specific and sensitive direct RIA for human urinary kallikrein has been developed and that both the Tos-Arg-OMe esterase and kininogenase assays measure human urinary kallikrein activity specifically, at least in the described circumstances.

Animals↗
PubMed1980

Kallikrein content of rat pancreatic acinar cells or islets by direct radioimmunoassay.

Recent reports have suggested that kallikreins may enzymatically convert proinsulin to insulin. The quantity of rat pancreatic kallikrein in isolated Islets of Langerhans, acinar cells and in whole pancreatic extracts was measured by direct radioimmunoassay and bioassay. Immunoreactive kallikrein content in acinar cells was 813 +/- 111 ng/mg protein (mean +/- S.E.M.). In whole pancreatic homogenates, it was 1303 +/- 213 ng/mg protein. Appreciable quantities of the enzyme were not detected in islets. Kallikrein activity as measured with a rat uterine bioassay had similar distribution. Because of the localization of kallikrein, it is unlikely that the enzyme is involved in the in vivo conversion of proinsulin to insulin.

Animals↗
PubMed1980

Role of endocrinological factors in the pathogenesis of idiopathic edema.

In order to investigate the etiology of idiopathic edema, clinical findings and endocrinological abnormalities were analyzed in twenty-seven patients, and the following results were obtained. An easy occurrence of subcutaneous bleeding and positive Rumpel-Leede phenomenon were observed in the majority of the patients. ADH, plasma renin activity and plasma aldosterone concentration in the patients did not show abnormalities following water loading in the supine position when compared with normal controls. But the results obtained in the present study suggested that they might contribute to water and sodium retention in the upright position. In the patients, plasma prolactin levels were not decreased, but rather increased and urinary excretion of kallikrein and kinin was reduced significantly after water loading in the upright position. Thus, prolactin and urinary kallikrein-kinin system might also contribute to water and sodium retention in idiopathic edema, directly or indirectly through the augmentation of the action of ADH and of aldosterone. It was concluded that the increased vascular permeability and endocrinological polyfactors play a role, in a cooperative fashion, in the mechanism of this disease.

Adult↗
PubMed1980

Acceleration of hypotension and development of stroke in the spontaneously hypertensive rat by unilateral ureteral obstruction.

Unilateral uareteral obstruction (UUO) in 6-week old male spontaneously hypertensive rats (6-w-SHR) accelerated the elevation of blood pressure and developed stroke with high frequency from 3 weeks after operation, whereas UUO had no effect in either 20-week old SHR or 6-week old normotensive Wistar Kyoto rats. Urinary protein excretion and plasma urea and renin concentrations in 6-w-SHR began to increase 2 weeks after UUO. Removal of the obstructed kidney in 6-w-SHR one week after UUO prevented the acceleration of hypertension, while the same treatment 2 weeks after operation did not. In the ureter-obstructed kidneys of 6-w-SHR, hydronephrotic atrophy was markedly observed already one week after operation, while in the opposite kidneys, hypertensive vascular lesions were manifested from the second week. These results indicate that with regard to reversibility of the hypertensive process, the obstructed kidney is more important in the early postoperative stages and the contralateral kidney more important later.

Animals↗
PubMed1979

Renal effects of propranolol, practolol and butoxamine in pentobarbital-anesthetized rats.

The renal effects of the beta-adrenergic blockers, propranolol, practolol and butoxamine, were examined in pentobarbital-anesthetized rats. All the beta-blockers, infused i.v., increased urine volume (V), urinary sodium excretion (UNaV) and p-aminohippuric acid clearance without change in inulin clearance. Indomethacin, an inhibitor of prostaglandin biosynthesis, did not affect the renal effects of these beta-blockers. Phentolamine abolished the renal effects of practolol, but not those of propranolol and butoxamine. Haloperidol abolished the renal effects of propranolol and butoxamine, but not those of practolol. A high correlation was found between the increased UNaV and the increased urinary phosphate excretion by butoxamine but not by propranolol and practolol. Therefore, it is suggested that alpha-adrenergic stimulation is involved in the mechanism of diuresis by practolol, a beta1-blocker, and that dopaminergic stimulation is involved in the diuresis caused by butoxamine, a beta2-blocker. Propranolol is similar to butoxamine, and partially similar to practolol.

Animals↗
PubMed1979

Measurement of urinary kallikrein acitvity by kinin radioimmunoassay.

We have established a simplified assay system for the measurement of urinary kallikrein activity by utilizing the sensitive and specific radioimmunoassay system of kinins previously reported from our laboratory. Kinins were generated by incubating urine samples (50 microliter) with kininogen (1500 ng) in the presence of kininase inhibitors, and the generated kinins were measured by radioimmunoassay. Since the cross reactivity of kininogen in the kinin radioimmunoassay system was not recognized at dose up to 1.0 microgram, the amount of untreated kininogen in the radioimmunoassay samples did not interfere with the measurement of kinins. This eliminated the necessity for a kininogen extraction procedure. A good linear correlation (r = 0.939, p less than 0.001) was observed between the urinary kallikrein activity determined by this assay system (kininogenase activity) and that by esterolytic acitvity. Urinary kallikrein activity was 3.3 +/- 0.9 microgram/min/24 hour urine (mean +/- SEM), 1.4 +/- 0.4 microgram/min/24 hour urine and 0.25 +/- 0.06 microgram/min/24 hour urine in 6 normal subjects, 7 patients with non-complicated essential hypertension and 4 patients with chronic renal failure, respectively. Thus, urinary kallikrein activity was significantly lower in the patients with essential hypertension (p less than 0.05) and the patients with chronic renal failure (p less than 0.01) than in the normal subjects.

Bradykinin↗
PubMed1979

A sensitive radioimmunoassay for the determination of plasma angiotensin II in human subjects.

A sensitive and specific radioimmunoassay for the determination of plasma angiotensin II was developed by using the antisera against synthetic angiotensin II in combination with labeled angiotensin II. This assay employs an acetone extraction procedure and detects as little as 0.8 pg per tube of angiotensin II. The mean (+/- S.E.) plasma angiotensin II concentration in 19 normal subjects was 14.4 +/- 1.8 pg/ml in a state of overnight fasting and recumbency. In 13 normal subjects, in whom 40 mg of furosemide was injected intravenously, plasma angiotensin II concentration before and after 30 and 120 minutes in an upright position was 14.6 +/- 2.2, 56.6 +/- 5.7 and 74.3 +/- 9.0 pg/ml, respectively. In 6 normal subjects, an infusion of isotonic saline, angiotensin II concentration reduced from 14.1 +/- 3.7 to 9.2 +/- 1.7 pg/ml. Thus, it was ascertained that the simplified radioimmunoassay method reported here using an acetone-petroleum ether extraction method was specific and highly sensitive.

Angiotensin II↗