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Biomedical subjects

S Fukuchi

Publications and source records attributed to S Fukuchi.

At least 199 records · Page 11Linked to original sources
PubMed1982

[Angiotensin-converting enzyme activity of the aorta in experimental hypertensive rats].

Angiotensin-converting enzyme activity of the aortic subcellular fractions (homogenate, mitochondria, microsomes and supernatant) was determined in normotensive and experimental hypertensive rats (1-clip, 1-kidney Goldblatt hypertensive; 1-clip, 2-kidney Goldblatt hypertensive and 2-clip, 2-kidney hypertensive rats). The systolic blood pressure markedly elevated in each group of experimental hypertensive rats, while it did not in normotensive rats. Angiotensin-converting enzyme activity was consistently high in the microsomal and supernatant fractions of the aorta in experimental hypertensive rats as well as in normotensive rats. However, the enzyme activity from each fraction of the aorta in 1-clip, 2-kidney Goldblatt hypertensive rats was significantly higher than that in normotensive and other experimental hypertensive rats. There was no significant difference in the enzyme activity among normotensive, 1-clip, 1-kidney Goldblatt hypertensive and 2-clip, 2-kidney hypertensive rats. The angiotensin-converting enzyme, widely distributed in subcellular fractions of the aorta, may play a possible role in the local control of vascular tone. It seems likely that increased angiotensin-converting enzyme activity in arterial tissue contributes to the initiation or development of hypertension in 1-clip, 2-kidney Goldblatt hypertension in rats.

Animals↗
PubMed1982

[The localization of aldosterone-producing adenoma on computed tomography--a comparative study with adrenal scintigraphy and plasma aldosterone concentration in the adrenal or renal vein].

The evaluation of computed tomography (CT) for detecting aldosterone-producing adenoma in primary aldosteronism was performed by comparison with adrenal scintiscan; determination of aldosterone in adrenal or renal veins, retroperitoneal pneumography and adrenal venography was reliable for diagnosis of adrenal tumors in pheochromocytoma or Cushing's syndrome, but not so effective for small adenoma of primary aldosteronism. An abdominal CT scan was performed on six patients with primary aldosteronism, one with idiopathic hyperaldosteronism and one with glucocorticoid responsive hyperaldosteronism; in an attempt to evaluate the utility of this noninvasive procedure. Diagnosis of hyperaldosteronism was made by demonstrating the elevated plasma aldosterone concentration and aldosterone secretion rate, normal excretion rate of urinary 17-OHCS and 17-KS, and low plasma renin activity. The CT scan correctly predicted unilateral adrenal adenoma in all the patients with primary aldosteronism of which the findings were identical to those demonstrated by surgery. The diameter of these tumors ranged from 10 X 7 X 6 to 19 X 17 X 14 mm. Also the CT scan in idiopathic hyperaldosteronism and glucocorticoid responsive hyperaldosteronism showed bilateral adrenal hyperplasia and bilateral normal adrenal glands, respectively. The pathological findings in these two cases disclosed the adrenal hyperplasia of zona glomerulosa and adrenal hyperplasia of zona subglomerulosa accompanied by a normal thickness of the adrenal gland, respectively. The precision of the CT scan, adrenal scintigraphy and determination of plasma aldosterone in the adrenal or renal veins were almost equal to the diagnosis of the localization of adrenal adenoma. It is concluded that the CT scan is a noninvasive and most useful method for the localization of aldosterone-producing adenoma and helpful in distinguishing adrenal adenoma from adrenal hyperplasia.

Adenoma↗
PubMed1982

[Clinical study on the angiotensin I-converting enzyme in human urine. (I) Partial purification, enzymic characteristics and excretion in normal subjects].

The angiotensin I-converting enzyme in normal human urine was partially purified with ammonium surfate (3.2M), DEAE-Cellulose ion exchange chromatography (0-0.5M NaCl gradient), and Sephadex G 200 gel filtration. The enzyme was separated into three forms which had different molecular weights of 700000, 290000 and 40000, respectively. The enzymic biochemical characteristics of these three enzymes, however, were identical with regard to their inhibitory effects (bradykinin potentiator c, arg-pro-pro, o-phenanthroline and EDTA), Cl- dependency, optimal pH (8.3) and temperature (37 degrees C), and Km value (2.3mM). The enzymic activity was determined in five normal subjects in three conditions of dietary sodium intake (51, 153 and 340mEq for 5 days, respectively). The enzymic activity correlated well with the concentration of the excreted sodium (r = 0.87, p less than 0.001). There was no significant relation between the enzymic excretion and the concentration of the excreted potassium, nor between the activity and the creatinine excretion. It is suggested that the origin of urinary angiotensin I-converting enzyme is the kidney, and that the enzyme might regulate sodium excretion in cooperation with renal kallikrein-kinin system.

Adult↗
PubMed1982

[The effect of trilostane, a new inhibitor of adrenal steroid biosynthesis, on blood pressure, plasma aldosterone and other steroid hormones, serum potassium and plasma renin activity in primary aldosteronism (author's transl)].

Six patients with primary aldosteronism (PA), one with idiopathic hyperaldosteronism (IHA), one with glucocorticoid responsible hyperaldosteronism (GRHA) and eight with essential hypertension (EH) were treated with trilostane (MWD-1822) (4 alpha, 5-epoxy-17 beta-hydroxy-3-oxo-5 alpha-androstane-2 alpha-carbonitrile), an inhibitor of adrenal steroid biosynthesis, for 9-47 days with a daily dose of 30-960 mg. Blood pressure decreased slightly and gradually from 30 min. to 360 min, plasma aldosterone (PAC) and cortisol concentration (F) decreased, and plasma dehydroepiandrosterone concentration (DHEA) increased 120 min. after the administration of a single dose of 120 mg of trilostane. In the patients with PA, IHA and GRHA on long term therapy with trilostane, blood pressure decreased, PAC and F were depleted, serum improved within normal limits and DHEA increased, but plasma progesterone concentration (Prog.) changed variously and plasma renin activity (PRA) remained suppressed. In the patients with EH, systolic pressure decreased in 5 out of 8 (under - 20 mmHg), and diastolic pressure decreased in 3 out of 8 (under - 10 mmHg), DHEA increased in all, but the changes in serum potassium, PAC, F, Prog. and PRA were various. There was no remarkable reaction after the administration of trilostane. It is concluded that trilostane is an effective inhibitor of 3-hydroxysteroid dehydrogenase in vivo and that it is useful in the treatment of primary aldosteronism and other hypertension due to hyperproduction of aldosterone.

Adult↗
PubMed1982

Two cases of low-renin hypertension thought to be due to excessive secretion of unknown mineralocorticoid.

Two patients with low renin hypertension showing an increased urinary excretion with 17-KS, with normal level of plasma deoxycorticosterone and no signs of virilization were reported. Dexamethasone induced reduction in blood pressure and elevation of serum K, in spite of acceleration of the renin-angiotensin-aldosterone system. Thus, it has been inferred that the hypertension was not associated with adrenogenital syndrome but was due to excessive production of an unknown mineralocorticoid.

17-Hydroxycorticosteroids↗
PubMed1982

Acute effect of cigarette smoking on serum angiotensin-converting enzyme activity in normal man.

The acute effect of cigarette smoking on serum angiotensin-converting enzyme activity was evaluated in 6 healthy subjects consisting of 4 non-smokers and 2 habitual smokers. Cigarette smoking resulted in rapid increases in serum converting enzyme activity in 5 of 6 subjects within 5 min. and the converting enzyme activity remained above the control value at 30 min. The increase in the enzyme activity of non-smokers was higher than that of habitual smokers at any time when the enzyme activity was determined. It is therefore suggested that cigarette smoke (or smoking) can cause the secretion of angiotensin-converting enzyme from the pulmonary endothelial cell, in which the enzyme may be produced, to the systemic circulation. It is also speculated that the increase in the enzyme activity may contribute to the initiation of cardiovascular changes associated with cigarette smoking.

Adult↗