Biomedical subjects
S Morimoto
Publications and source records attributed to S Morimoto.
[Calcitonin concentration in the cerebrospinal fluid in patients with medullary thyroid carcinoma--passing of calcitonin through the blood-brain barrier].
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[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.
[Radiologic study of persistent fetal circulation syndrome].
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Serum calcium regulating hormones in the perinatal period.
To clarify perinatal vitamin D metabolism, we measured 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D [24,25(OH)2D], 1,25-dihydroxyvitamin D [1,25(OH)2D], calcium (Ca), phosphorus (P), parathyroid hormone (PTH), and human calcitonin (CT) in paired maternal, cord, and infant serum. Cord serum 25OHD was significantly lower than the maternal level, and cord serum 24,25(OH)2D was also significantly below the maternal concentrations. Maternal, cord, and infant serum 1,25(OH)2D, on the other hand, was significantly higher than the normal adult level. The serum PTH was low, but the CT concentration was high in the cord. Cord serum Ca and P levels were significantly higher than maternal. The reason for the elevated circulating 1,25(OH)2D level in the perinatal period is uncertain, and we speculate that the possible factors are gonadal steroids, placental lactogen, prolactin, and CT. In addition, serum 24,25(OH)2D and 1,25(OH)2D concentrations are under some control by the fetus.
Normal serum 1,25-dihydroxyvitamin D in patients with medullary carcinoma of the thyroid.
Serum calcium, phosphorus, calcitonin, parathyroid hormone, 25-hydroxyvitamin D (25OHD), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] were measured in 6 women and 2 men with medullary carcinoma of the thyroid, 22 normal subjects, 5 patients with chronic renal failure, and 5 patients with primary hyperparathyroidism. Serum 1,25-(OH)2D levels were significantly higher in patients with primary hyperparathyroidism and lower in patients with chronic renal failure than in normal subjects. In patients with medullary carcinoma of the thyroid, the serum calcitonin levels were elevated, but the parathyroid hormone and 1,25-(OH)2D levels were within normal ranges. The serum 25OHD levels were not significantly different in any group. It is concluded that chronic elevation of serum calcitonin has no effect on the serum 1,25-(OH)2D level.
Calcitonin in plasma and cerebrospinal fluid from normal subjects and patients with medullary thyroid carcinoma: possible restriction of calcitonin by the blood-brain barrier.
Calcitonin (CT) was measured by RIA in samples of plasma and cerebrospinal fluid (CSF) obtained simultaneously from 27 normal volunteers and 8 patients with medullary thyroid carcinoma to examine the extent of penetration of CT across the blood-brain barrier. CT concentrations in plasma and CSF were 68.2 +/- 25.1 pg/ml (mean +/- SD; range, less than 25-110) and 38.5 +/- 12.1 pg/ml (range, less than 25-56), respectively, in normal subjects and 5,650 +/- 4,120 pg/ml (range, 980-21,100) and 36.1 +/- 11.1 pg/ml (range, less than 25-45), respectively, in patients with medullary thyroid carcinoma. No significant difference was observed in the mean concentrations of CT in CSF from normal subjects and that from patients with medullary thyroid carcinoma. The concentration of CT in CSF from patients with medullary thyroid carcinoma was only 0.05-2.5% the concentration of CT in plasma. Moreover, there was no significant correlation between the concentrations of CT in plasma and CSF from normal subjects, from patients with medullary thyroid carcinoma, or when normal and patient groups were combined. It is concluded that penetration of CT from blood in CSF is minimal.
Effect of vitamin E-deficiency on renin release from renin granules.
This study was undertaken to investigate the effects of vitamin E-deficiency on renin release from isolated renin granules. Male Wistar rats were fed either a control or a vitamin E-deficient diet. Renin granules were prepared from the kidney cortex homogenate by a discontinuous sucrose density gradient centrifugation. Renin activity was measured by radioimmunoassay and lipid peroxidation was estimated by means of the thiobarbituric acid test. The intake of vitamin E-deficient diet for 4 weeks resulted in a decrease in alpha-tocopherol content in renin granules, accompanied by an increased level of endogenous lipid peroxides. When the renin granules were incubated at 37 degrees C, the rate of renin release from the granules in vitamin E-deficient group was significantly higher than that in the control group. These results indicate that vitamin E exists in renin granule membranes and functions in maintenance of membrane integrity by blocking the lipid peroxidation.
High molecular weight renin in the mouse kidney.
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A comparative study on the measurement of urinary kallikrein in the rat.
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Renin release and lipid peroxidation in renin granules of the rat.
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Radioimmunoassay of urinary calcitonin in normal subjects and in patients with medullary carcinoma of the thyroid.
A simple technique for measuring urine calcitonin (CT) was established using a sensitive radioimmunoassay (RIA) system for plasma human calcitonin (hCT). To extract urinary CT, urine samples were fractioned by gel chromatography on a column (0.8 x 20 cm) of Bio Gel P-2. Recovery of synthetic (1-32)hCT was 86.1 +/- 6.2% and the intra- and inter-assay coefficients of variation in RIA were 5.9 and 8.2%, respectively. Dilution curves of the urinary CT after gel-filtration were parallel with the standard curve. In 11 patients with medullary carcinoma of the thyroid (MCT), the CT levels of the urine (in ng/mg Cr) were 3.4 to 20.8 times higher than those of the plasma (in ng/ml), and a significant positive correlation (r = 0.93, P less than 0.001) was obtained between the urinary and plasma levels of CT in these 11 patients. In 32 normal subjects, the CT levels of the urine (in pg/mg Cr) were only 0.41 to 5.1 times of those of the plasma (in pg/ml), and a weak positive correlation (r = 0.408, P less than 0.05) was obtained between these two levels. However, urinary CT level in normal subjects apparently reflected a rise in endogenous plasma hCT in response to calcium infusion (4 mg/kg B.W. for 1 min) and that of exogenous plasma CT when synthetic (1-32)hCT (500 micrograms for 1 min) was injected intravenously. Following gel filtration on a Bio Gel P-30 1.5 x 80 cm column, larger molecular forms of CT than (1-32)hCT were found in the urine not only patients with MCT but also of normal subjects after infusion of calcium or synthetic (1-32)hCT. It is concluded that measurement of urine CT is useful not only for diagnosis of MCT but also for evaluating CT metabolism in normal subjects.
Effect of the catecholestrogen 2-hydroxyestradiol on the renin-angiotensin system in the rat.
The effects of the catecholestrogen 2-hydroxyestradiol (250 and 500 micrograms/day, each for 7 days) on plasma renin substrate (PRS), activity (PRA) and concentration (PRC) were studied in male rats as compared with those of estradiol (250 micrograms/day, for 7 days) and vehicle alone (for 7 days). Pre-treatment levels of PRS, PRA, PRC and the PRA/PRC ratio were similar in four groups. After vehicle treatment, PRS, PRA, PRC and the PRA/PRC ratio remained unchanged. Estradiol treatment, however, produced an increase in PRS, an increase in PRA but no change in PRC. The PRA/PRC ratio after estradiol treatment was high. On the other hand, 2-hydroxyestradiol treatment caused no increase in PRS at a daily dose of 250 micrograms and a slight but significant increase in PRS at a daily dose of 500 micrograms. This treatment also produced increases in PRA as well as PRC at the two daily doses. These increases in PRA and PRC tended to be higher at a daily dose of 500 micrograms than at a daily dose of 250 micrograms. The PRA/PRC ratios after 2-hydroxyestradiol treatment were unaltered at the two daily doses. It is concluded that, while 2-hydroxyestradiol is less active in increasing PRS than estradiol, the compound is capable of increasing PRC.
Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.
A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a two-month hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] ALL. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] ALL. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5 mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance. These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.
A case of male pseudohermaphroditism due to 17 alpha-hydroxylase deficiency.
A case of male pseudohermaphroditism due to 17 alpha-hydroxylase deficiency is described. A 24-year-old woman with a quadriplegic attack exhibited primary amenorrhea, lack of secondary sexual characteristics, hypertension, hypokalemic alkalosis and hyporeninemia. She had female external genitalia together with a 46 XY karyotype and intraabdominal testes. No uterus was found. Endocrinological studies showed low levels of urinary pregnanetriol, plasma cortisol and urinary 17-OHCS, high level of urinary pregnanediol, and markedly elevated plasma levels of deoxycorticosterone, corticosterone and 18-hydroxycorticosterone with a low level of plasma and urinary aldosterone. Plasma ACTH was high. Plasma and urinary androgens and estrogens were low in the presence of a high level of plasma and urinary gonadotropins. Treatment with 2-0.5 mg/day of dexamethasone improved the abnormal plasma levels of the corticosteroids and normalized the blood pressure, serum potassium and PRA. The addition of estrogen (ethinylestradiol, 0.05 mg daily) to dexamethasone treatment produced only poor development of the breasts six months later.
Potential spaces of the mediastinum: CT pneumomediastinography.
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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.
[Serum human calcitonin level in patients with non-thyroidal cancer (author's transl)].
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