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Biomedical subjects

T Kusaka

Publications and source records attributed to T Kusaka.

At least 91 records · Page 5Linked to original sources
PubMed1976

Interaction of dopamine, methyldopa and reserpine in the sympatho-adrenal system in essential hypertension.

1. The interactions of dopamine, reserpine and methyldopa on blood pressure of normal subjects and of those with essential hypertension were examined. 2. When biosynthesis of noradrenaline from dopamine was blocked by reserpine, dopamine induced a prominent depressor effect in essential hypertension. 3. The long-term treatment with methyldopa induced a marked potentiateion of the pressor action of domapine in hypertension, although no significant pressor response was found in normal subjects. 4. It is suggested that methylnoradrenaline may accumulate in peripheral nerve endings of patients with essential hypertension in comparison with normal subjects, and this accumulated methylnoradrenaline potentiates the pressor response to dopamine in essential hypertension.

Adult↗
PubMed1976

Solubilization of diglyceride acyltransferase from the membrane of Mycobacterium smegmatis.

Diglyceride acyltransferase [acyl-CoA : 1,2-diacylglycerol O-acyltransferase, EC 2.3.1.20] was found to be localized in the membrane of Mycobacterium smegmatis, and this enzyme could be solubilized from the membrane by treatment with aqueous acetone. The solubilized enzyme required either 1,2-diolein or 1, 3-diolein as an acceptor for palmitoyl-CoA. The apparent Km value for 1,2- or 1,3-diolein and that for palmitoyl-CoA were about 1.4 X 10(-5) M and 6 X 10(-6) M, respectively. Several sulfhydryl reagents were inhibitory to the enzyme activity, suggesting the existence of a thiol group(s) in its active site. The solubilized enzyme, which was more labile than that membrane-bound one, could be stabilized to some extent with antichaotropic salts such as phosphate, pyrophosphate, and sulfate.

Acyltransferases↗
PubMed1976

Elevated plasma renin activity in aortitis syndrome.

Plasma renin activity (PRA) was measured in 38 cases of aortitis syndrome. The values of resting peripheral vein blood PRA were 32.2 +/- 4.2 (SE) mmug/ml. These values were 3 times higher than those of normal subjects. Hypertension due to renal arterial stenosis was observed in 18 cases. Their resting PRA values were 41.2 +/- 6.0 mmug/ml, while in the remaining 20 patients without renovascular hypertension those values were 24.2 +/- 5.4 mmug/ml. The patients belonging to aortic arch type or extensive type had 2 times higher PRA values than those of abdominal type. The patients with stenosis or obstruction of common carotid arteries had significantly higher PRA values than the patients without these lesions. Hyperresponse of renin secretion to upright posture was also observed in the same patients with carotid artery stenosis. Abnormal renin release in Takayasu's arteritis disappeared after denervation of the carotid sinus nerve. The present study suggests that the unstable state of carotid sinus reflex is the main cause for the hypersecretion of renin.

Adolescent↗
PubMed1975

Diurnal variation of the human urinary TRH excretion measured by radioimmunoassay.

Urine TRH was estimated by the radioimmunoassay which was accomplished according to the method of Bassiri and Utiger. Minimum detectable dose of TRH was 25 pg and recovery of TRH ranged from 72% to 112% in our laboratory. Intraassay coefficients of variation were 5.4% to 14.0% and interassay variations were 10.6% to 15.0%. Of the TRH analogues tested, only two (Ser-His-Pro-NH2, Thr-His-Pro-NH2) had potent reactivity to anti-TRH serum in large dose of 100 ng/tube. Urine samples were kept at -20 degrees C after adjusted to pH 3.0 because the inactivation of TRH in urine was markedly dependent on temperature and pH value. Using this radioimmunoassay, diurnal variation of the urinary TRH excretion at regular intervals in normal subjects was observed. Peak TRH excretion occurred around early morning, while minimum of the excretion was observed around noon. Total urinary TRH excretion of 24 hours was 817-1579 ng (M+/-SE: 1241+/-89 ng) in normal subjects. In patients with chronic renal failure, urinary excretions of TRH was obviously lower than those of normal subjects.

Adolescent↗