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Biomedical subjects

R Takeda

Publications and source records attributed to R Takeda.

At least 415 records · Page 23Linked to original sources
PubMed1982

Effect of bile acids on 1,2-dimethylhydrazine-induced colon cancer in rats.

The effects of intercepting a part of the enterohepatic circulation of bile acids by ileal resection or bypass on the quantitative and qualitative changes of fecal bile acids were investigated in rats, and the relationship of these changes to the development of DMH-induced colon cancer was studied. The daily fecal total bile acid level was increased in all intercepted groups, especially those with long resection and exclusion. Total bile acid levels played a greater role in the development of DMH-induced colon cancer than did primary or secondary bile acid levels individually. Our findings suggest that bile acid acts as a promoter in the development of colon cancer.

1,2-Dimethylhydrazine↗
PubMed1982

[Total blood volume in essential and secondary hypertension].

To study the role of volume factors in the pathogenesis of hypertension, total blood volume (TBV) was determined in 43 patients with essential hypertension, 10 with primary aldosteronism, 5 with Cushing's syndrome, 5 with renovascular hypertension and 23 age-matched normotensives. The radioisotope (131I) labeled plasma tracer technique was employed under conditions of constant sodium intake (200mEq/day). The TBV values obtained were expressed as % normal against the predicted values according to the formulae of Fujita and his co-workers. The results were as follows: (1) TBV was increased in patients with primary aldosteronism. (2) In essential hypertensive patients, with either normal or low plasma renin activity, TBV was normal. (3) There was no increment of TBV in patients with Cushing's syndrome. These results suggest that expanded intravascular volume plays a major role in the mechanism of hypertension with suppressed plasma renin activity in primary aldosteronism, whereas other unknown factors may be related to the causes of hypertension in patients with essential hypertension and Cushing's syndrome.

Adult↗
PubMed1982

Urinary prostaglandins and kallikrein in the course of acute renal failure.

To examine the role of prostaglandins and the kallikrein system in the recovery from acute renal failure, we studied the sequential changes in urinary prostaglandins and kallikrein after the onset of oliguria. The six patients studied had acute tubular necrosis of the vasomotor type. Urinary PGE2, PGF2 alpha, the PGF2 alpha-main urinary metabolite, 6-keto-PGF1 alpha and TXB2 were all measured by radioimmunoassay. Urinary kallikrein was assayed by means of hydrolytic activity using a chromogenic tripeptide substrate. Following onset of diuresis, urinary PGE2 excretion was increased to normal, parallel to the increase in urine volume. In contrast, the ratio of urinary PGF2 alpha/PGE2 peaked at the onset of diuresis, indicating a relative increase in PGF2 alpha production at this time. Prior to this peak, urinary kallikrein concentrations reached the highest levels, suggesting a close connection with renal prostaglandin metabolism. On the other hand, changes in PGF2 alpha-MUM, 6-keto-PGF1 alpha and TXB2 were not found. These results indicate that there may be an interlocking acute alteration of the kallikrein-prostaglandin system occurring immediately before the resolution of oliguria, although the role of the acute shift to PGF2 alpha production observed needs further study.

Acute Kidney Injury↗
PubMed1982

Hypouricemia due to renal urate wasting. Two types of tubular transport defect.

We present 2 patients associated with hypouricemia. Serum uric acid levels were 1.6 and 1.3 mg/100 ml, and the ratios of urate clearance to creatinine clearance were 34.1 and 39.4%, respectively, while glomerular filtration rates (GFR) were normal. In the pyrazinamide (PZA) suppression test these 2 patients showed a different response of urate excretion. In the first patient urate excretion showed only a slight decrease following PZA. The load of benzbromarone did not increase urate excretion significantly. This patient is considered to have a defect of urate reabsorption in the proximal tubule, resulting in renal uricosuria. The second patient, on the contrary, showed nearly complete suppression of urate excretion after PZA. Uricosuric response to benzbromarone was far less than in the normal subjects. The suppression rate of urate excretion following PZA in benzbromarone-induced uricosuria was similar to the value of the normals. These results suggest that the latter had a defect of postsecretory reabsorption of urate in the tubule.

Adult↗
PubMed1982

Lecithin: cholesterol acyl transfer rate in hypothyroidism and hyperthyroidism.

The initial rate of lecithin: cholesterol acyl transferase and serum concentration of lipids were determined in euthyroid, hypothyroid and hyperthyroid subjects. In hyperthyroid subjects, the serum levels of total and free cholesterol were significantly lower than in normal subjects and the fractional lecithin: cholesterol acyl transfer rate was significantly higher than in normal subjects. The molar lecithin: cholesterol acyl transfer rate was also higher than in normal subjects, but not significantly. The free cholesterol/total cholesterol ratio in hypothyroid females and the serum levels of triglyceride and free fatty acid in hypothyroid male were significantly higher than in normal subjects. The fractional lecithin: cholesterol acyl transfer rates in hypothyroid females were significantly lower than in normal females. After treatment of the thyroid disease the fractional and molar lecithin: cholestorol cholesterol acyl transfer rate approached the normal values. There was a positive correlation between fractional and molar lecithin: cholesterol acyl transfer rate and thyroxine. These results suggest that thyroid hormone influences the cholesterol esterification through the activation of lecithin: cholesterol acyltransferase.

Adult↗
PubMed1982

The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients.

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.

Acromegaly↗
PubMed1982

Aldosterone responsiveness to angiotensin II after sodium restriction in subjects with low renin essential hypertension.

Plasma aldosterone (PA) responses to sodium restriction (25 mEq sodium/day for 4 days) and to graded angiotensin II (AII) infusions (2, 4 and 8 ng/kg/min each for 30 min) during a low sodium intake were studied in 14 subjects with low renin essential hypertension (LREH) versus 16 normotensive subjects. The PA response to sodium restriction in relation to changes in plasma renin activity (PRA) was estimated by the ratio of PA increment to PRA increment after sodium restriction (delta PA/delta PRA). In 8 of 14 LREH subjects, whose delta PA/delta PRA ratios were normal, the PA responses to the graded AII doses were similar to those in the normotensive subjects. However, in the remaining 6 LREH subjects whose delta PA/delta PRA ratios were high the PA responses to the graded AII doses were greater. Apparently some LREH subjects, whose delta PA/delta PRA ratios after sodium restriction were high, have an abnormally enhanced aldosterone responsiveness to AII under the condition of low sodium intake.

Adult↗
PubMed1982

Role of prostaglandins in the aldosterone response to ACTH in sodium depleted human subjects.

It is well established that the response of plasma aldosterone to ACTH is enhanced in the sodium depleted state. The mechanisms for this phenomenon are not clear, however, and the present study was undertaken to determine the possible participation of endogenous prostaglandins. ACTH, 250 ug by i.m. administration, was given to 10 human subjects pretreated in four different ways: 1. Control, receiving a 200 mEq per day sodium diet; 2. Sodium depletion (60 mEq/day sodium plus furosemide) plus indomethacin; 3. Sodium depletion plus indomethacin plus captopril; and 4. Sodium depletion plus captopril. Only in the last group, in which the prostaglandin cyclooxygenase inhibitor, indomethacin, was not given during the sodium depletion, did an exaggerated aldosterone response to ACTH occur (an increase of 468% compared with an increase of 182% during control, P less than 0.005). The angiotensin converting enzyme inhibitor, captopril, did not effect this response. Thus, endogenous prostaglandins appear to be of far greater importance than the renin-angiotensin system in mediating the increased aldosterone response to ACTH administration during the sodium depleted state in man.

Adrenocorticotropic Hormone↗