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Biomedical subjects

M Oka

Publications and source records attributed to M Oka.

At least 649 records · Page 36Linked to original sources
PubMed1986

Effect of the novel orally active angiotensin converting enzyme inhibitor alacepril on cardiovascular system in experimental animals.

Effects of 1-[(S)-3-acetylthio-2-methylpropanoyl]-L-prolyl-L-phenylalanine (alacepril, DU-1219) a new orally active angiotensin converting enzyme (ACE) inhibitor, on cardiovascular system in experimental animals were examined. In conscious renal hypertensive dogs, alacepril (3 mg/kg p.o.) caused a marked reduction in systolic and diastolic blood pressure (SBP and DBP) and total peripheral vascular resistance (TPR), but did not change significantly heart rate (HR), cardiac output (CO), stroke volume (SV), cardiac work (CW) and electrocardiogram (ECG). Captopril (3 mg/kg, p.o.) showed similar changes in cardiovascular parameters as alacepril. In anesthetized open-chest normotensive dogs, alacepril (3-100 micrograms/kg/min for 10 min, i.v. infusion) tended to decrease DBP and TPR, but did not change significantly CO, stroke work (SW), left ventricular end diastolic pressure (LVEDP), dp/dt and HR. Captopril also showed similar effects but these changes were greater in extent than those of alacepril. In conscious renal hypertensive rats, alacepril did not affect the regional cerebral blood flow in the frontal cortex and the dorsal hippocampus after single (3 and 10 mg/kg) and successive (3 mg/kg/d for 7 days) oral administration. Captopril (10 mg/kg) significantly decreased blood flow in the frontal cortex after single oral administration. In conscious normotensive dogs, alacepril (3 and 30 mg/kg p.o.) increased renal plasma flow (RPF), urine volume (UV), urinary sodium excretion (UNaV) and urinary Na+/k+ ratio, but did not change glomerular filtration rate (GFR) and urinary potassium excretion (UKV). Captopril (3 and 30 mg/kg p.o.) also showed similar changes as alacepril. These effects of alacepril on cardiovascular system resemble those of captopril and might be considered as a favourable profile for the antihypertensive agent.

Animals↗
PubMed1985

Muscarinic receptor-mediated increase in cytoplasmic free Ca2+ in isolated bovine adrenal medullary cells. Effects of TMB-8 and phorbol ester TPA.

The change in cytoplasmic free calcium, [Ca2+]i in isolated bovine adrenal medullary cells during stimulation by acetylcholine (ACh) in Ca2+-free incubation medium was measured using the fluorescent Ca2+ indicator quin2. ACh (1-100 microM) caused an increase in [Ca2+]i by mobilization of Ca2+ from the intracellular pool. Nicotine (10 microM) did not increase [Ca2+]i in the absence of extracellular Ca2+. Pretreatment of the cells with atropine (10 microM) completely inhibited ACh-induced increase in [Ca2+]i, whereas pretreatment with hexamethonium (100 microM) did not. The intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), inhibited ACh-induced increase in [Ca2+]i. The activator of protein kinase C 12-O-tetradecanoylphorbol-13-acetate (TPA), but not its 'inactive' analog 4 alpha-phorbol-12,13-didecanoate (PDD), also inhibited ACh-induced increase in [Ca2+]i. These findings suggest that in bovine adrenal medullary cells, stimulation of muscarinic ACh receptor causes an increase in [Ca2+]i by mobilizing Ca2+ from the intracellular pool and that protein kinase C is involved in 'termination' or 'down regulation' of this response.

Acetylcholine↗
PubMed1985

Phorbol ester stimulates catecholamine synthesis in isolated bovine adrenal medullary cells.

In isolated bovine adrenal medullary cells, the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA), an activator of protein kinase C, stimulated [14C]catecholamine synthesis from [14C]tyrosine, but not from [14C]DOPA. This stimulatory effect of TPA on [14C]catecholamine synthesis was not dependent upon extracellular Ca2+, and TPA did not affect the uptake of 45Ca2+ or the release of catecholamine by the cells. TPA also did not affect the intracellular cyclic AMP (cAMP) level. 4 alpha-Phorbol 12, 13-didecanoate, which is not an activator of protein kinase C, did not stimulate the synthesis of [14C]catecholamine from [14C]tyrosine. The stimulatory effect of TPA on [14C]catecholamine synthesis was additive with that of carbamylcholine, but not with that of dibutyryl cAMP (DB-cAMP). From these results, it was suggested that protein kinase C is involved in the regulation of tyrosine hydroxylase activity and that this regulatory mechanism might be similar to that involving cAMP.

Adrenal Medulla↗
PubMed1985

Quantitative analysis of development of mitochondrial ultrastructure in differentiating mouse hepatocytes during postnatal period.

Between birth and 10 days of age, the volume density (volume/unit cytoplasmic volume) of the matrix, and the surface density (area/unit cytoplasmic volume) of the inner membrane and cristae increased in both periportal and perihepatic hepatocytes, and did not differ significantly between the cells of the two zones. After 10 days of age, however, the volume density of the matrix decreased in perihepatic cells and remained unchanged in periportal cells, and, therefore, it became greater in periportal cells than in perihepatic cells in 20-day-old and adult animals. The surface density of the inner membrane and cristae decreased in the cells of both zones. Further, the hepatocyte volume increased markedly, especially in perihepatic zones between 20 days of age and the adult. The results show that, in postnatally differentiating hepatocytes, mitochondria are likely to develop during early postnatal period, then the structural heterogeneity of mitochondria arises, and hepatocyte volume increases markedly during late postnatal period after weaning. Thus, the process of postnatal hepatocyte differentiation includes such several phases of development.

Aging↗
PubMed1985

Urinary lumichrome-level catabolites of riboflavin are due to microbial and photochemical events and not rat tissue enzymatic cleavage of the ribityl chain.

The occurrence of 7- and 8-carboxylumichromes as a significant fraction of riboflavin-derived material in rat urine has led to a reexamination of tissues for possible enzymatic activity that could contribute to cleavage at position 10 of the D-ribityl chain of the vitamin. For this, homogenates were incubated in the dark under various conditions with pure [2-14C]riboflavin with and without cofactors prior to extractions with phenol for flavins or chloroform for lumichromes, and high pressure liquid chromatography was used to separate and to quantitate all radioactive compounds. Only unmodified riboflavin and small amounts of flavin mononucleotide (FMN) were found even though the level of detection of known derivatives including 10-(2'-hydroxyethyl)flavin and lumichrome was shown to be extremely sensitive. Hence, rat tissue per se does not appear responsible for significant cleavage of the D-ribityl chain of riboflavin. Rather such cleavage to the lumichrome level must result from the known actions of intestinal microflora and potentially from photolysis.

Animals↗
PubMed1985

Inhibitory effect of colchicine and vinblastine on transport of glucagon receptors to the plasma membrane in cultured rat hepatocytes.

The role of microtubules in the regulation of glucagon receptors on cultured rat hepatocytes was studied. Antimicrotubular reagents, colchicine and vinblastine, did not affect the binding of 125I-labelled glucagon to hepatocytes at 4 degrees C. At 20 and 37 degrees C, however, the reagents reduced the binding after 60 or 90 min of incubation. Scatchard analysis indicated that the reduction in the binding was due to loss of glucagon-receptor populations. If hepatocytes were preincubated with both unlabelled glucagon and the reagents at 37 degrees C, the binding of the ligand to the cells decreased markedly after a certain delay. The reagents did not inhibit the internalization of the ligand in the cells until 30 min of incubation at 37 degrees C. The results suggest that the microtubule system plays a role in the transport of glucagon receptors to the plasma membrane, which is followed by their internalization.

Animals↗
PubMed1985

Treatment with danazol of ureteral obstruction caused by endometriosis.

A case of unilateral ureteral obstruction in extensive endometriosis in a 21-year-old patient is reported. The present patient received danazol therapy following conservative surgery, and restoration of the renal function was achieved 5 months after initiation of the danazol administration.

Adult↗