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Biomedical subjects

T Eto

Publications and source records attributed to T Eto.

At least 361 records · Page 20Linked to original sources

Renin response to furosemide differs with the routes of administration in health men.

Plasma renin activity (PRA) was serially determined 0, 15, 30, 60 and 120 min following administration of furosemide in a dose of 40 mg intravenously (i.v.) and 80 mg orally (p.o.) at a one week interval in 10 healthy men. Following i.v. furosemide administration, PRA increased rapidly and reached a plateau level of 6.1 +/- 1.0 ng/ml/h (222 +/- 44% of the control), at 15 min and remained at about the same level throughout the remaining period of the study. In contrast, PRA increased progressively to a maximum level of 5.5 +/- 0.7 ng/ml/h (285 +/- 53% of the control), 120 min after p.o. furosemide. In case of p.o. furosemide, the increase in PRA was dependent on the doses used per body weight, and was significantly correlated with the cumulative sodium excretion by itself, or the cumulative sodium excretion adjusted by either the leanness index or the body surface area. Such relationships were not apparent after i.v. furosemide. These findings suggest that the response of renin release to furosemide in healthy men differs with the routes of administration and renin release with p.o. furosemide may be largely due to a net sodium loss, while mechanism(s) other than sodium loss may be involved in the early hypersecretion of renin with i.v. administration of furosemide.

Administration, Oral↗

Ultrastructural types of cell in adrenal cortical adenoma with primary aldosteronism.

By means of electron microscopy, three types of cell were identified in the adrenal cortical adenomas obtained by surgery from three patients with primary aldosteronism. They were zona glomerulosa-type cells, compact cells and clear cells. The former two types of cell were quite similar to those found in the zona glomerulosa and the zona reticularis respectively. The clear cell with large lipid vacuoles possessed mitochondria similar to those found in the outer zona fasciculata. The ultrastructure of the vacuoles was rather complex and their relationship to those in the zona fasciculata cell was not clear. Glycogen particles in the beta-form, which were present in the zona glomerulosa and reticularis cell but not in the zona fasciculata cell, were observed within the cytoplasm of this tumour cell. The clear cells of the tumours were therefore considered to possess features of both the zona glomerulosa and the zona fasciculata cell.

Adenoma↗

Preparation and characterization of an active lysozyme derivative: Kyn 62-lysozyme.

A novel method for the preparation of Kyn 62-lysozyme, in which tryptophan 62 is replaced by kynurenine, is reported. Hen egg-white lysozyme was ozonized in aqueous solution to yield one N'-formylkynurenine residue and deformylated with hydrochloric acid in frozen solution at -10 degrees C. Crude Kyn 62-lysozyme was purified by affinity and Bio Rex 70 chromatography successively. Kyn 62-lysozyme retains affinity for chitin and is essentially an active enzyme with a slightly weakened but distinct catalytic activity. After this modification, the enzyme activity was changed differently depending on the kind of substrate. At the individual optimum pH's, lytic activity was largely retained (80% active), but the catalytic efficiency for hydrolyzing glycol chitin was relatively low (30% active). Lysis of M. lysodeikticus cell suspensions was optimally catalyzed by Kyn 62-lysozyme at pH 6.2 and at 0.088 ionic strength. These values are lower by 1.3 pH unit and 0.04 ionic strength, respectively, than those of intact lysozyme. The optimum pH and ionic strength for the hydrolysis of neutral substrates were scarcely affected. These results suggest the significance of electrostatic interaction in the lysis of lysozyme. Relatively limited loss of activity induced by modification of the 62nd residue, which is thought to participate directly in the binding of the substrate at subsite C, is discussed on the basis of the similarity of side chain structure in tryptophan and kynurenine.

Amino Acids↗

Acute arteriolar lesions of rat intestine caused by kidney extract.

Lysosomal fraction of renal cortical extract, which showed high renin activity, and equipressor dosis of synthetic angiotensin II amide were administered into one-hour nephrectomized rats. Sixty minutes after the sustained elevation of 20 mmHg in mean arterial pressure by each pressor substance, the rats were sacrificed and the intraperitoneal organs were fixed. Five minutes prior to the administration of each pressor substance ferritin solution, as a test substance for vascular permeability, was intravenously injected. Medial changes in the arterioles in the intestinal submucosa were observed by electron microscopy. In angiotensin II group early lytic lesions of the muscle cells were limited to the single muscle cells. Ferritin particles were rarely found in the media. In lysosomal fraction group the lytic lesions were more advanced. Some regions of the media exhibited focal loss of smooth muscle cells manifesting focal medial necrosis. Ferritin particles were distrubuted in some areas of the necrotic media. The results suggested that the kidney extract with high renin content contained substance(s) to produce both medial necrosis and plasma insudation into the media of the arterioles.

Angiotensin II↗

Early vascular changes in the intestine of bilaterally nephrectomised rats.

Ultrastructural changes in the arterioles of the intestinal submucosa were observed in rats 20 to 24 hr after bilateral nephrectomy. Sham-operated rats served as controls. The changes of arterial pressure after the nephrectomy or sham operation was measured directly through carotid artery cannulation, and analysed by the paired t-test. Ferritin was injected intravenously into two rats in each group 60 min. before fixation in order to trace plasma insudation into the arteriolar wall. Mean blood pressure was 102 +/- 9 and 112 +/- 6 mm Hg (mean +/- S.E.), before and after the nephrectomy, respectively. The latter was significantly higher than the former, though it remained in the normotensive range. It was also higher than that in control rats after sham operation. In sham-operated rats, there were neither vascular lesions nor evidence of increased leakage of ferritin into arteriolar walls. Arterioles from the nephrectomised rats, on the other hand, exhibited foci of smooth muscle cell necrosis characterised by cellular fragmentation and the deposition of fibrinoid and electron-dense granules. The fibrinoid was of two types of axial periodicity, i.e., 20--23 nm and 16--17 nm, respectively. Dense granules, 13--90 nm in diameter, were encountered mainly between the basement membrane and plasma membrane of smooth muscle cells. Though scanty fibroblasts were seen, there was no infiltration of mononuclear cells in the adventitia accompanying medial necrosis. Ferritin particles accumulated in the necrotic foci of the media in high concentration, and were seen in endothelial gaps, within the cytoplasm and in palsmalemmal vesicles of the endothelial cells. The main pathway of ferritin insudation into the media was considered to be by way of endothelial gaps.

Animals↗

Increased capillary permeability in muscularis layer of rat intestine caused by kidney extract.

Kidney extract and synthetic angiotensin II were injected into bilaterally nephrectomized rats in dosages capable of raising the mean arterial pressure by about 20 mmHg. Changes in ultrastructure and permeability for ferritin molecules were then examined in capillaries located in muscularis layer of the intestinal walls. Kidney extract with a high renin content was obtained from the renal cortex of rats by means of stepwise centrifugation methods. Animals injected with saline served as controls. In rats receiving kidney extract tissue edema was observed in the spaces around the blood and lymphatic capillaries. In these spaces ferritin molecules accumulated in high concentration indicating plasma protein leakage. Ferritin molecules within the endothelium were restricted within plasmalemmal vesicles, but were not found within interendothelial junctions or within the cytoplasmic matrix. Morphometric analysis of vesicular transport in the endothelial cells revealed a significant increase in labeling rate for the vesicles with ferritin molecules. These results suggest that the kidney extract contains substance(s) which increase capillary permeability for plasma proteins at least via increased vesicular transport, resulting in tissue edema.

Angiotensin II↗

Blood fibrinolytic activity and fibrinoid necrosis of small arteries in the rats treated with renal cortical extract.

In order to determine the role of fibrinolytic system in the production of fibrinoid necrosis, blood fibrinolytic activities were measured in the rats nephrectomized and administered with the subcellular fractions (lysosomal or microsomal fraction) of the rat kidney cortical extract. Tissue plasminogen activator was present in both fractions and blood fibrinolytic activity was increased in the rats so treated. But fibrinoid necrosis in pancreatic and mesenteric small arteries was observed only in those administered lysosomal fraction. Direct relationship between the increase of blood fibrinolytic activity and the aggravation of the vascular degeneration could not be observed in this experiment.

Animals↗

An electron microscope study on permeability in cerebral venules in the rats with hypertensive encephalopathy.

Hypertensive encephalopathy was induced in the rat by clipping one renal artery and contralateral nephrectomy. The possible changes of vascular permeability of the cerebral blood capillaries and venules were investigated by using ferritin as a tracer. The uninephrectomized rats served as controls. In controls, ferritin was never seen in the basement membranes, within plasmalemmal vesicles on the basal surface of the endothelium, or in endothelial cell junctions of cerebral capillaries and venules up to 180 min after the injection. In venules of the brain in rats with hypertensive encephalopathy, a number of ferritin particles appeared in the basement membrane in 60 min after the injection. Many plasmalemmal vesicles in the endothelial cells of venules were labeled with ferritin. However, ferritin particles were never found in the endothelial cell junctions. The results suggested that leakage of macromolecules, such as serum proteins, occurred in venules mainly by increased vesicular transport.

Animals↗