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Biomedical subjects

T Kono

Publications and source records attributed to T Kono.

At least 361 records · Page 20Linked to original sources
PubMed1980

Evidence that insulin causes translocation of glucose transport activity to the plasma membrane from an intracellular storage site.

The glucose transport activity of fat cells was assayed in a cell-free system. The activity was solubilized and incorporated into egg-lecithin liposomes. The carrier-mediated glucose transport activity was estimated by subtracting the cytochalasin B-insensitive component from the total glucose uptake activity of the modified liposomes. When a crude microsomal preparation from fat cells was fractionated by sucrose density gradient centrifugation, two transport activities (peaks A and B) were separated. Peak A coincided with the peak of 5'-nucleotidase, a marker of the plasma membrane. Peak B appeared to coincide with the peak of UDPGal:N-acetylglucosamine galactosyltransferase, a marker of the Golgi apparatus. Peak A was considerably smaller than peak B under basal conditions. When cells were exposed to 1 nM insulin for 5 min before homogenization, the height of peak A increased whereas that of peak B decreased. Insulin had no significant effect on the galactosyltransferase activity. The Km values of glucose transport facilitated by the activities in peaks A and B were both approximately 10-15 mM. These results imply that insulin facilitates translocation of the transport activity from an intracellular storage site to the plasma membrane.

Adipose Tissue↗
PubMed1980

Effects of ageing and gonadal steroid hormones on prolactin concentrations in the anterior pituitary of the chicken.

1. Effects of ageing and gonadal steroid hormones on pituitary prolactin (PRL) concentration in the chicken were investigated. 2. No difference was found in the qualitative electrophoretic patterns of the anterior pituitary homogenates at different ages and between the sexes. 3. Pituitary PRL concentrations in males were generally higher than in females. 4. Pituitary PRL concentrations in castrated immature cockerels were higher than in intact birds, while PRL concentration was depressed by the injection of testosterone propionate or oestradiol benzoate. 5. Prolactin concentration in intact immature cockerels was decreased by daily injection of testosterone or oestradiol for 3 weeks but not by injection of the hormones for 1 week.

Aging↗
PubMed1980

Biological activity of des-Asp1-angiotensin I in man.

The biological activity of des-Asp1-angiotensin I (des-Asp1-AI) was studied in five normal men. An iv infusion of 300 ng (258 pmol)/kg.min des-Asp1-AI caused a remarkable rise in blood pressure, a decrease in PRA, and an increase in plasma aldosterone concentration. The pressor and steroidogenic actions of this dose of des-Asp1-AI were slightly less than those of 100 ng (111 pmol)/kg.min des-Asp1-angiotensin II [Angotensin III (AIII)] which we reported previously and were abolished by a single oral administration of 100 mg of a converting enzyme inhibitor, SQ 14225. These results indicate that in man, as in animals, a rise in blood pressure and an increase in plasma aldosterone concentration after an infusion of des-Asp1-AI are entirely due to the actions of AIII converted from this nonapeptide, and that the conversion rate of des-Asp1-AI to AIII in normal men is less than 43%. This is much less than the conversion rate of angiotensin I to angiotensin II. It seems unlikely that des-Asp1-AI has physiological significance in the human renin-angiotensin-aldosterone system.

Aldosterone↗
PubMed1980

Effects of diltiazem hydrochloride on pressor and steroidogenic actions of angiotensins and norepinephrine in man.

The effect of diltiazem hydrochloride (DTZ), a calcium-antagonist, on pressor and steroidogenic action of angiotensin II (AII), angiotensin III (AIII) and norepinephrine (NE) was studied in 5 normal men. AII, AIII and NE were infused intravenously for 50 min from 0900 hr at a rate of 20 ng/kg/min, 100 ng/kg/min and 200 ng/kg/min, respectively. DTZ was infused intravenously alone or in combination with each of these pressor substances at a rate of 1 mg/min from 0910 hr to 0930 hr. DTZ alone did not cause significant changes in blood pressure (BP) and plasma aldosterone concentration (P1 Aldo). On the other hand, DTZ combined with AII, AIII or NE significantly inhibited the rise in BP induced by these pressor substances. DTZ also inhibited the NE-induced increase in P1 Aldo, whereas it did dot alter AII-, or AIII-induced increase in P1 Aldo. These results indicate that in normal men pressor actions of AII, AIII and NE are calcium-dependent and calcium ions are also involved in NE-induced increase in P1 Aldo.

Adult↗
PubMed1979

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.

Adult↗
PubMed1979

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.

Adrenocorticotropic Hormone↗