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Biomedical subjects

K Morii

Publications and source records attributed to K Morii.

67 records · Page 4Linked to original sources

Methods for enzymatic and colorimetric determinations of D-erythrulose (D-tetrulose).

The specific determinations of D-erythrulose by enzymatic assay or colorimetric method, which permit the quantitative determination of between 20 and 400 nmol of the sugar, are described. Enzymatic determination of D-erythrulose made use of the D-erythrulose reductase purified from beef or chicken liver, which catalyzes specifically the reduction of D-erythrulose with concomitant conversion of NADH to NAD+. The colorimetric microdetermination of erythrulose could be carried out by utilizing the phenol-sulfuric acid reaction under low temperature. These methods are simple, rapid, and sensitive, and give reproducible results.

Animals↗

Changes in DOPAC and 5-HIAA after acute cerebral hemorrhage induced by hypertonic glucose solution (i.p.)--in vivo voltammetry study.

Intraperitoneal injection of hypertonic glucose solution induced intracranial hemorrhage in rats. Simultaneously determined plasma norepinephrine exponentially increased followed by death. Using in vivo voltammetry, the present study was undertaken to estimate the relationship between neurochemical parameters and intracranial bleedings induced by hypertonic glucose injection. When placed in a solution of dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5-HIAA), electrically pretreated carbon fiber electrodes produced a 3 distinct peaks. Peak 1 and 2 refer to the extracellular fraction of ascorbic acid and DOPAC. Peak 3 refers to that of 5-HIAA. The peaks of the voltammograms obtained in vivo from different areas of the brain are similar to those observed in vitro using DOPAC and 5-HIAA solutions. Electrodes implanted in the ventricular CSF showed that DOPAC increased immediately after glucose injection, while 5-HIAA did not change significantly. When the electrode was inserted into the putamen, 5-HIAA exponentially increased followed by death, whereas DOPAC showed only a small change. It was presumed that the stroke-induced major oxidizable compounds are different in the lateral ventricle and the putamen. These results suggest that during cerebral bleeding, plasma norepinephrine increases accompanied with a potentiation of the central DOPAC and 5-HIAA system in rats.

3,4-Dihydroxyphenylacetic Acid↗

[Effects of new antihypertensive agent, 2-[4-(n-butyryl)-homopiperazine-1-ul]-4-amino-6, 7-dimethoxy-quinazoline (E-643), on blood pressure, urinary sodium excretion and urinary norepinephrine excretion rate in stroke-prone, spontaneously hypertensive rats].

Present study was undertaken to elucidate the effects of E-643, on blood pressure, urinary electrolyte (U-Na, U-K) and catecholamines excretion rates in stroke-prone spontaneously hypertensive rats (SHRSP). An attempt was also made to clarify the effects of E-643 on plasma catecholamine concentration and sympathetic efferent nerve discharges including renal and adrenal nerve activity. E-643 (10 mg/kg/day X 4 weeks, p.o.) administered SHRSP (E-643 SHRSP) produced a significant hypotensive effect as compared with sex-age matched nondrug control SHRSP (control SHRSP). Both U-Na and U-K in E-643 SHRSP increased significantly as compared with those of control SHRSP. Urinary norepinephrine content (U-NE) also increased significantly in E-643 SHRSP. Plasma NE concentration tended to increase in E-643 SHRSP. While, plasma epinephrine (E) concentration decreased significantly in E-643 SHRSP. E-643 did not produce any significant effects on both sympathetic renal nerve activity and adrenal nerve activity in SHR. The changes induced by exogenous administered NE (blood pressure rise, tachycardia and the change in sympathetic nerve activity) were antagonized by pretreatment of E-643 in SHR. It was demonstrated that therapeutic doses of E-643 did not seem to produce any significant effect on central nervous system. These findings suggest that E-643 is a peripherally acting alpha 1 antagonist with natriuretic effect.

Animals↗

[Effects of a new vasodilator, budralazine on water drinking activity, plasma norepinephrine, plasma angiotensin II, plasma arginine vasopressin, plasma serotonin concentration, urinary aldosterone excretion rate and urinary catecholamine excretion rate in rats].

Present study was undertaken to elucidate the effects of a new vasodilatating antihypertensive drug, budralazine on water drinking behavior and humoral factors including plasma norepinephrine (NE), angiotensin II (A II), arginine vasopressin (AVP), serotonin (5-HT) concentrations, urinary aldosterone and catecholamine excretion rates. After oral budralazine administration (10 mg/kg/day, p.o., for 7 days), systolic tail blood pressure of Wistar Kyoto rats (WKY) decreased significantly. While, heart rate and water drinking activity of WKY significantly increased. Urinary catecholamine excretion rate did not change after oral administration of budralazine (10 mg/kg and 100 mg/kg/day, p.o.; for 7 days). However, significant increase in urinary aldosterone excretion rate was demonstrated. Both plasma A II and NE concentrations tended to increase after oral administration of budralazine (100 mg/kg/day). Plasma AVP and 5-HT concentrations were not influenced by budralazine. These findings suggest that budralazine acts on renin angiotensin aldosterone system as compared to that in the sympathetic nervous system.

Aldosterone↗

[Effect of metoprolol on water drinking activity in Wistar Kyoto rats].

The study was undertaken to elucidate the effect of beta 1 adrenoceptor blocking agent, metoprolol, on water drinking activity in Wistar Kyoto rats (WKY). Both 7 day (10mg/kg/day) oral administration of metoprolol and propranolol did not produce any changes in the systolic blood pressure of WKY. However, metoprolol produced a significant decrease in heart rate in WKY. Neither the propranolol treated rats nor the control (non-drug group) rats showed any significant changes in heart rate. Heart rates were significantly changed in the metoprolol group as compared with the other two groups. This finding reconfirms that metoprolol has beta 1 selectivity. Drinking activity, an indicator of central nervous function, did not change after metoprolol administration. Power spectral analysis of water drinking activity did not reveal any changes in rhythm in respect to periodicity in the metoprolol group. Although water drinking activity is synchronized with urinary catecholamine and aldosterone excretion rates, urinary catecholamine and aldosterone excretion rates did not change after metoprolol administration. These findings suggest that it is the beta 1 adrenergic blocking action of a bradycardia-producing dose of metoprolol that prevented any change in water drinking behavior in WKY.

Aldosterone↗

Membranous lipodystrophy: a clinicopathological study of six cases.

Membranous lipodystrophy apparently is a new disease, first reported and named by Nasu and associates 31 in 1971. We have collected six cases of this disease. The initial manifestation was articular pain at adolescence. Symmetrical changes in the bones of the extremities then appeared and the disease seemed to progress slowly with age. The younger patients exhibited only skeletal pain or fractures, while the older patients had some neuropsychiatric changes. Three of the patients died in middle age. The cystic bone lesions contained a yellow, lipid-like substance which histologically showed a characteristic membranocystic appearance. Electron microscopic study showed unique features, but biochemical analysis of the substance did not reveal a definable abnormality.

Adult↗

The effect on methamphetamine on the mRNA level for 14.3.3 eta chain in the human cultured cells.

14.3.3 protein, a brain-specific protein, is an activator of tyrosine and tryptophan hydroxylases, key enzymes for biosynthesis of dopamine and serotonin. In this article, we describe cloning of cDNA for human brain 14.3.3 eta chain and expression of 14.3.3 eta chain mRNA in some human cultured cells. The cloned cDNA is 1730 bp long and contains 191 bp of a 5'-noncoding region, the complete 738 bp of coding region, and 801 bp of a 3'-noncoding region, containing three polyadenylation signals. This cDNA encoded a polypeptide of 246 amino acids (M(r) 28,196). Furthermore, using in situ hybridization histochemistry, the expression of mRNA for this protein was examined in the rat central nervous system. In situ hybridization histochemistry indicated that 14.3.3 eta chain mRNA is detected not only in the monoamine-synthetic neurons, but also in other neurons in the discrete nuclei, which synthesize neither cathecholamine nor serotonin. Northern blot analysis demonstrated that the addition of methamphetamine into the cultured medium increased the mRNA level for 14.3.3 eta chain in U-251 cells, but did not increase that of GFAP.

14-3-3 Proteins↗

Effect of SM-2470, a newly synthetized alpha 1-adrenoceptor antagonist, on sympathetic nerve activity in anesthetized rats.

The newly synthetized alpha 1-adrenoceptor antagonist, SM-2470 (4-amino-2-[4-(bicyclo(2,2,2)oct-2-ene-5-carbonyl)-1-piperazinyl]-6,7- dimethoxyquinazoline hydrochloride), is a prazosin-like quinazoline derivative. The present study was undertaken to elucidate the effect of SM-2470 on sympathetic nerve activity and baroreceptor afferent nerve activity in anesthetized rats. Intravenous administration of SM-2470 (10, 30 and 100 micrograms/kg) produced a dose-dependent reduction of mean arterial pressure without any significant change in heart rate. SM-2470 caused decreases in both renal and cardiac sympathetic nerve activity along with this hypotension. Preganglionic adrenal nerve activity and aortic depressor nerve activity were also decreased by SM-2470. When equi-hypotensive doses of SM-2470 and clonidine were compared, the sympathoinhibitory potency of SM-2470 was less than that of the centrally acting antihypertensive drug, clonidine. Pretreatment with SM-2470 (30 micrograms/kg, i.v.) shifted the methoxamine-induced pressor response curve to the right. These findings suggest that SM-2470 may possess a central sympathoinhibitory action. This central action may play a role in its anti-tachycardic effect and may be substantially responsible for the hypotensive action.

Adrenergic alpha-Antagonists↗