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Biomedical subjects

M Murai

Publications and source records attributed to M Murai.

At least 325 records · Page 18Linked to original sources
PubMed1981

[Effects of benzoylcholine on ChE activity in rabbit and rat brain and erythrocytes (author's transl)].

Cholinesterase (ChE) hydrolyzing acetylcholine (ACh) in vivo can be classified into two groups. The ChE localizing in brain and erythrocytes is known as ChE and hydrolyzes ACh and acetyl-beta-methylcholine (MeCh) but not benzoylcholine (BzCh). The ChE localizing in liver and serum is termed pseudo ChE and hydrolyzes ACh and BzCh but not MeCh. Effects of BzCh, a specific substrate of pseudo ChE on true ChE in brain mitochondria and erythrocytes of rabbit and rat were studied. The ChE activities in rabbit brain with ACh and MeCh as substrates were decreased to 1/4 and 1/3 of the control activities by addition of 10 mM BzCh, respectively. The pS curve for ChE in rabbit brain and erythrocytes with ACh and MeCh as substrates markedly decreased by addition of 3 mM of BzCh. The inhibitory effect of BzCh was reversible and competitive, as assessed by a Lineweaver-Burk plot method. BzCh protected by the irreversible inactivating effect of true ChE by DEP. These results suggest that BzCh is not hydrolyzed by true ChE but does have an affinity for the active center of true ChE.

Acetylcholine↗
PubMed1981

Spironolactone bodies in aldosteronomas and in the attached adrenals. Enzyme histochemical study of 19 cases of primary aldosteronism and a case of aldosteronism due to bilateral diffuse hyperplasia of the zona glomerulosa.

The formation of spironolactone (S) bodies, eosinophilic laminated cytoplasmic inclusions, is induced in the aldosterone-producing cells of the human adrenal cortex after the administration of spironolactone. The aim of this study was to define the enzyme histochemical characteristics of S bodies, S-body-containing cells, and the apparently hyperplastic zona glomerulosa (zG) of adrenal tissues attached to aldosteronomas. S bodies were found in 14 of 19 aldosteronomas, in 10 of 19 adrenal tissues attached to aldosteronomas, and in the adrenal tissues in a patient with aldosteronism due to bilateral diffuse zG hyperplasia. The S bodies themselves exhibited most intense 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) activity but did not exhibit glucose-6-phosphate dehydrogenase (G6PD), NADP-dependent isocitrate dehydrogenase (NADP-ICDH), or succinate dehydrogenase (SDH) activity, confirming histochemically the origin of S bodies in the smooth endoplasmic reticulum. In two adenomas, S bodies were found to be surrounded by reaction products of acid hydrolase but were not found in the other adenomas and the remaining adrenal tissues. S-body-containing cells, irrespective of being neoplastic or not, showed enhanced 3 beta HSD, G6PD, and NADP-ICDH activity and weak SDH activity (Type I pattern of enzyme activity). Though zG was hyperplastic in most of the adrenal tissues attached to the adenomas, zG cells that did not contain S bodies showed the opposite pattern (Type II pattern) of enzyme activity (ie, weak 3 beta HSD, G6PD, and NADP-ICDH activity and intense SDH activity), in contrast to those in the adrenal tissues in a patient with aldosteronism due to bilateral diffuse zG hyperplasia (which showed the Type I pattern). The results are consistent with the view that hyperplastic zG cells, except S-body-containing cells, in the case of aldosteronoma are not hyperfunctioning. The latter cells may have enhanced but possibly abortive steroidogenic activity.

Adenoma↗
PubMed1980

[Studies on the mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome (author's transl)].

The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.

Adenoma↗
PubMed1978

Antiandrogenic effects of spironolactone: hormonal and ultrastructural studies in dogs and men.

A decrease in the level of plasma testosterone and an increase in the level of plasma progesterone were noted after spironolactone had been administered for 20 days in 5 patients with prostatic carcinoma, as well as in 8 male dogs. Electron microscopic observation disclosed myelin-like bodies in the cytoplasm of Leydig and adrenocortical cells in dogs, contributing to a resolution of the mode of antiandrogenic action of spironolactone.

Adrenal Glands↗