Biomedical subjects
F Oseko
Publications and source records attributed to F Oseko.
Effects of angiotensin I-converting enzyme inhibitor, SQ 14225, in nomal men.
Effects of an orally active angiotensin I-converting enzyme inhibitor, SQ 14225, on the actions of angiotensin I (AI) infused intravenously for 120 to 390 min were studied in 5 normal men. When 20 ng/kg/min of AI infusion was started immediately after a single oral administration of 100 mg of SQ 14225, a significant rise in blood pressure (BP) was observed for the first 15 min, but BP began to fall from 17 min and returned to the pretreatment level at 45 min. This BP level continued at least to 120 min and in one subject to 180 min. In this subject BP began to rise again from 185 min and reached the level of 15 min at 390 min. Plasma AI level increased gradually from 45 min. At 15 min plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased, but then PRA began to increase and PA began to decrease. At 120 min the values of PRA and PA were similar to the pretreatment values. In one subject plasma AI and PRA began to decrease and PA began to increase after 120 or 180 min. On the other hand, in the 5 men sole AI infusion caused a continued BP rise, PRA decrease and PA increase, and sole SQ 14225 administration caused increases in plasma AI and PRA and a decrease in PA but no BP change. From these results it was concluded that complete blockade and partial inhibition of AI conversion by 100 mg of oral SQ 14225 lasted for about 2.5 and 6.5 hr, respectively and that BP rise, PRA suppression and aldosterone stimulation after AI infusion were entirely due to the actions of angiotensin II converted from AI.
Lack of inhibition of ACTH-induced aldosterone stimulation by des-asp1-,ileu8-angiotensin II in man.
In 5 normal men an intravenous injection of 0.5 mg of synthetic 1-24 ACTH caused a significant increase in plasma aldosterone and a simultaneous intravenous infusion of 600 ng/kg/min of des-asp1-, ileu8-angiotensin II (AIIIA) did not inhibit this increase. Since this dose of AIIIA is known to inhibit an angiotensin II-induced increase in plasma aldosterone in normal men, the present results suggest that the ACTH-induced aldosterone stimulation is mediated by an adrenocortical receptor which is different from angiotensin II receptors.
[Angiotensin II analogue and essential hypertension].
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[Basic studies on prolactin kit [Daiichi] and its application to clinics (author's transl)].
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[Angiotensin I converting enzyme inhibitor and angiotensin II antagonist].
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Bladder carcinoma associated with ectopic production of gonadotropin.
A rare incidence of a primary gonadotropin-producing bladder carcinoma in which gynecomastia appeared in the terminal stage was encountered in a 76-year-old Japanese male. There was a good probability that the symptoms of hormonal activity were due to chorionic gonadotropin (hCG), since its whole molecule, beta- and alpha-subunits were detected by radioimmunoassay in the blood, urine, and the tissue from the malignant neoplasm, and the plasma and urine estrogens were elevated. Recent papers concerning the synthesis of hCG-like material by neoplastic cells are reviewed and the implication of the measurement of beta- and alpha-subunits of hCG in various neoplastic diseases are discussed. Other characteristic profiles of plasma hormonal levels are also discussed in this case.
Diabetic retinopathy in acromegaly.
A study was made of diabetic retinopathy in acromegaly. 10 of 15 patients with acromegaly had diabetes mellitus, and 3 of the 10 showed diabetic retinopathy. 2 of them had a diabetic family history. 1 patient with a diabetic family history had retinopathy of state IIIa in Scott's classification, and the other 2 showed a few microaneurysms and/or punctate hemorrhages in the macula. Diabetes mellitus and diabetic retinopathy in acromegaly showed no correlation with the duration of acromegaly and diabetes mellitus, age, or growth hormone level. No diabetic cataract was found in the present series. It was concluded that diabetic retinopathy due to secondary diabetes mellitus is usually slight or moderate. Diabetes mellitus with severe retinopathy is probably primary diabetes due to a genetic defect, and secondary diabetes may be different in nature from the primary disease.
Inhibition of angiotensin III action by DES-ASP1-,ILEU8-angiotensin II in man.
In 5 normal men intravenous infusion of 600 ng/kg/min of des-asp1-ileu8-angiotensin II (AIIIA) inhibited a rise in blood pressure as well as increase in plasma aldosterone caused by an intravenous infusion of 20 or 100 ng/kg/min of des-asp1-angiotensin II (angiotensin III, AIII). This result and our previous study on simultaneous infusions of 600 ng/kg/min of AIIIA and 20 ng/kg/min of angiotensin II (AII) in the same 5 normal men demonstrate that this dose of AIIIA antagonizes AIII and AII on the adrenal cortex as well as peripheral arterioles and that AIIIA has the same degree of inhibitory effect on the aldosterone-stimulating action of AIII and on that of AII in man.
Hypothalamo-pituitary-testicular axis in men undergoing chronic intermittent hemodialysis.
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[Bartter's syndrome].
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Biological activity of high dose of des-asp 1-, ileu 8-angiotensin II in man.
The biological activity of high doses of des-asp 1-, ileu 8-angiotensin II (AIIIA) was studied in man. In 5 normal men an intravenous infusion of 600 ng/kg/min of AIIIA for 30 min caused a slight rise in blood pressure, a decrease in plasma renin activity and an increase in plasma aldosterone. This dose inhibited pressor and steroidogenic actions of angiotensin II infused into the same 5 normal men at a rate of 20 ng/kg/min for 30 min. These results are considerably different from our previous report using lower dose (200 ng/kg/min) of AIIIA and indicate that in man AIIIA has both agonist and antagonist activities on the peripheral arterioles as well as on the adrenal cortex.
[Low renin hypertension and aldosterone].
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Blood pressure fall by angiotensin II antagonist in patients with Bartter's syndrome.
Intravenous infusion of 600 ng/kg/min of 1-sarcosine, 8-isoleucine-angiotensin II, an angiotensin II antagonist, caused a marked blood pressure fall and a decrease in plasma aldosterone in 3 patients with Bartter's syndrome. These results indicate that proximal cause of Bartter's syndrome is an arteriolar hyporesponsiveness to angiotensin II and that this angiotensin II analogue has an antagonist activity on peripheral arterioles as well as adrenal cortex.
Biological activity of des-Asp1-,Ileu8-angiotensin II (Ileu8-angiotensin III) in man.
Biological activity of ileu8-angiotensin III (AIIIA) was studied in man. In 5 normal men intravenous infusion of 200 ng/kg/min of AIIIA for 30 minutes from 0900 h had no effect on blood pressure (BP) but caused a decrease in plasma renin activity (PRA) and an increase in plasma aldosterone (PA). This dose did not inhibit pressor and steroidogenic actions of angiotensin II (AII) infused into the normal men at a rate of 20 ng/kg/min for 30 minutes. In 3 patients with Bartter's syndrome 260-1,200 ng/kg/ min of AIIIA infusion for 30 minutes from 0900 h had no effect on BP but caused decreases in PRA and PA. These results indicate that in man AIIIA has no pressor action and no antagonistic effect on pressor action of AII but has PRA-lowering and aldosterone-stimulating effects. Antagonistic effect of AIIIA on steroidogenic action of AII was also shown in patients with Bartter's syndrome but not in AII-treated normal men. This may be due to the difference of administered dose of AIIIA.
[Clinical application of angiotensin II derivatives].
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