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Biomedical subjects

M Gotoh

Publications and source records attributed to M Gotoh.

At least 523 records · Page 29Linked to original sources
PubMed1982

Matrical inclusions of peroxisomes induced by clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethyl-aminoazobenzene.

The response of peroxisomes to clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethylaminoazobenzene was examined histochemically (using the 3,3'-diaminobenzidine reaction) and electron microscopically. Morphometrical examinations revealed that the number of peroxisomes correlated well with the intensity of the histochemical reaction. Preneoplastic hepatocytes which responded to clofibrate with a marked proliferation of peroxisomes showed no matrical inclusions or merely matrical plates in very low incidence in the proliferated peroxisomes. The cells that exhibited a moderate proliferation of peroxisomes showed formation of peroxisomal matrical inclusions in high incidence. The inclusions were matrical plates and tubules showing the same fine structures as those found in 2-acetylaminofluorene carcinogenesis. These peroxisomal inclusions were absent in the cells which responded to clofibrate with no or only a slight increase in the number of peroxisomes. It is suggested that these varieties of peroxisomal changes might reflect the progress of preneoplastic phases of the cells.

Animals↗
PubMed1982

[Echocardiographic findings of a patient with cardiac amyloidosis and left ventricular outflow obstruction].

This report described 56-year-old male with cardiac amyloidosis, whose echocardiographic and hemodynamic findings suggested hypertrophic obstructive cardiomyopathy. M-mode echocardiography demonstrated asymmetric septal hypertrophy (2.1 cm/1.6 cm), systolic anterior motion of the mitral valve, and pericardial effusion. Two-dimensional echocardiography revealed marked hypertrophy of the septum and papillary muscles with characteristic fine grannular sparkling appearance of the myocardium. Bilateral heart catheterization showed normal hemodynamics except a pressure gradient of 35 mmHg within the left ventricular outflow tract. Moreover, no hemodynamic evidence of restrictive cardiomyopathy was observed. Myocardial biopsy was performed at the time of pericardiectomy, and diffuse amyloid deposits were identified between myocardial fibers. It is of particular interest that cardiac amyloidosis presented the form of ventricular hypertrophy associated with left ventricular outflow obstruction, probably due to uneven deposition of amyloid.

Amyloidosis↗
PubMed1982

Primary culture of preneoplastic hepatocytes from rats treated with 2-acetylaminofluorene and clofibrate: relationship between resistance to dimethylnitrosamine and responsiveness of peroxisomes.

Hepatocytes of 2-acetylaminofluorene-induced hyperplastic nodules of rats treated with clofibrate were transferred to primary culture after dispersion by a collagenase perfusion technique. After 48-hr treatment with dimethylnitrosamine (DMN), the resistance to the agent of the cells forming rod-shaped peroxisomes was examined. Catalase activity of the DMN-resistant cells was also determined. At concentrations of 10(-3)M and 10(-4)M DMN, the resistant cell population of hepatocytes with rod-shaped peroxisomes was larger than that of the cells without abnormal peroxisomes. On the other hand, the catalase activity of the attached cells that remained after DMN treatment decreased as the concentration of DMN was increased. The cells showing a stronger induction of the enzyme activity were found to be more sensitive to the cytotoxicity of DMN and they became detached from the culture dishes.

2-Acetylaminofluorene↗
PubMed1982

Hepatocytes with extraperoxisomal catalase in rats fed 3'-methyl-4-dimethylaminoazobenzene.

Histochemical and cytochemical studies were done to further characterize the preneoplastic hepatocytes with extraperoxisomal catalase (EPC-cells) that were found in the livers of rats fed 3'-methyl-4-dimethylaminoazobenzene. Catalase activity was demonstrated cytochemically to be localized in nuclear matrices, hyaloplasm, and peroxisomal matrices of EPC-cells. It is suggested that an impairment of peroxisome formation is involved in the altered intracellular distribution of catalase. Administration of clofibrate increased the catalase activity in EPC-cells. To examine the preneoplastic nature of EPC-cells, activities of glucose-6-phosphatase (G6Pase) and gamma-glutamyl transpeptidase (GGT) were examined, since changes in the activities of these enzymes have been used as markers of putative preneoplastic cells. In the present study, neither weak G6Pase activity nor positive GGT activity was considered to be a consistent feature of EPC-cells. However, available evidence suggests that EPC-cells are one of the carcinogen-induced cell populations with altered phenotypes.

Animals↗
PubMed1981

[The effects of dexamethasone and captopril on plasma aldosterone response to exogenous angiotensin II in normal men (author's transl)].

The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.

Adult↗
PubMed1981

[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)].

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.

Adult↗
PubMed1981

Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients.

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.

Adult↗
PubMed1981

Effect of sodium intake on brain angiotensin-converting enzyme activity in spontaneously hypertensive rat.

The effect of sodium intake on angiotensin-converting enzyme activity in five areas of the brain (the cerebral cortex, midbrain, striatum, thalamus and hypothalamus) was studied in normotensive, spontaneously hypertensive and stroke-prone spontaneously hypertensive rats. The enzyme activity was significantly higher in the hypothalamus than in other areas of the brain of spontaneously hypertensive rats. Sodium intake resulted in a significant rise of the enzyme activity in the midbrain of spontaneously hypertensive rats and also in the midbrain and the striatum of stroke-prone spontaneously hypertensive rats. In normotensive rats, however, there was no significant difference in the enzyme activity in any area of brain between the control and the salt-treated group. It is likely therefore that a high circulating sodium level increases angiotensin-converting enzyme content of the brain in spontaneously hypertensive rats, and it is suggested that the increased converting-enzyme activity may play a role in development of hypertension induced by sodium loading.

Animals↗
PubMed1981

Brain angiotensin-converting enzyme activity in experimental hypertensive rats.

Angiotensin-converting enzyme (ACE) activity was measured in six areas of the brain of normotensive and experimental hypertensive rats; one-clip, one-kidney (1-c, 1-k) and one-clip, two-kidney (1-c, 2-k) Goldblatt hypertensive (GH) rats. ACE activity was consistently high in the thalamus of normotensive and both 1-c, 1-k and 1-c, 2-k GH rats. However, the enzyme activity in the hypothalamus of 1-c, 2-k GH rats was significantly higher than that of normotensive rats, while there was no significant difference in the enzyme activity between normotensive and 1-c, 1-k GH rats. These results demonstrate that in 1-c, 2-k GH rats, increased ACE activity in the brain may play a central role in the hypertension.

Animals↗
PubMed1981

Dose-dependent enhancing effect of phenobarbital on hepatocarcinogenesis initiated by diethylnitrosamine in the rat.

Sequential feeding of various dose levels of phenobarbital (PB) after diethylnitrosamine (DENA) administration revealed that the enhancing effect of PB on hepatocarcinogenesis was dose-dependent. The highest dose level of PB, 0.2% in the diet, greatly enhanced the formation of tumors larger than 5mm in diameter. Tumors obtained in the 0.2% PB feeding group were more numerous and larger in size than those in th 0.01, 0.05, and 0.1% PB feeding groups. although it took longer, the enhancing effect of 0.01% PB feeding was evident when DENA had been administered for 3 weeks, while the same dose level of PB clearly enhanced hepatocarcinogenesis when the carcinogen had been given for 5 weeks.

Animals↗
PubMed1981

Estimation of resistance to dimethylnitrosamine of normal hepatocytes, hyperplastic nodule cells and hepatoma cells of rats in primary culture.

Normal hepatocytes, hyperplastic nodule cells and hepatoma cells of rats induced by 2-acetylaminofluorene treatment were transferred to primary culture. After exposure of the cells to dimethylnitrosamine (DMN) at concentrations of 10(-2) M, 10(-3) M, and 10(-4) M for 48 hr, the attached cells which remained on the dishes in a flattened shape were counted. Resistance to DMN was expressed as the percentage of the attached cells relative to the control without DMN treatment. The percentages increased in the order of normal hepatocytes, hyperplastic nodule cells and hepatoma cells.

Animals↗