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Biomedical subjects

M Yanase

Publications and source records attributed to M Yanase.

At least 91 records · Page 5Linked to original sources
PubMed1987

The urinary excretion of frusemide and its metabolites by kidney transplant patients.

Urine from 5 renal transplant recipients treated with frusemide was analyzed for unchanged frusemide (F), glucuronidated frusemide (G) and 4-chloro-5-sulfamoylanthranilic acid (CSA) by HPLC. In 3 recipients, whose renal function recovered steadily and whose hepatic function was normal throughout, the ratio of frusemide to its metabolites, F/(F + G + CSA), increased steadily in conjunction with the recovery of renal function. In one patient, who received frusemide 200-400 mg/day i.v., the urinary CSA concentration was 64-102 micrograms X ml-1. In 2 patients who experienced shock and/or hepatic dysfunction after transplantation, the F/(F + G + CSA) ratio fluctuated.

Adult↗
PubMed1986

Activators of protein kinase C inhibit sodium transport in A6 epithelia.

To evaluate the role of protein kinase C in sodium transport via amiloride-sensitive sodium channels, we studied the effect of activators of protein kinase C on short-circuit current in epithelia formed by A6 cells in culture. In A6 epithelia, short-circuit current is equivalent to net sodium transport and is blocked by low concentrations of amiloride added to the solution bathing the apical surface. After any of four different activators of protein kinase C [phorbol 12,13-dibutyrate (20 ng/ml), phorbol 12-myristate 13-acetate (20 ng/ml), 1-oleoyl-2-acetylglycerol (50 micrograms/ml), and mezerein (10 ng/ml)] was added to the solution bathing the apical surface, short-circuit current fell, and electrical resistance rose. Nystatin added to the apical solution reversed the inhibition of short-circuit current, indicating that activators of protein kinase C inhibited transport at amiloride-sensitive sodium channels in the apical plasma membrane. Under some conditions, the activators also stimulated amiloride-insensitive short-circuit current. The ion transport represented by the amiloride-insensitive short-circuit current appears to be the result of basal to apical transport of chloride, but this has not been established conclusively.

Amiloride↗
PubMed1986

Adenosine 3',5'-cyclic monophosphate stimulates chloride secretion in A6 epithelia.

Basal and aldosterone-stimulated short-circuit current (Isc) of A6 epithelia are known to be equivalent to net apical to basal Na flux and are completely inhibited by 0.05 mM amiloride added to the solution bathing the apical surface of the epithelium. In the absence of amiloride, the Isc stimulated by adenosine 3',5'-cyclic monophosphate (cAMP) is also equivalent to net apical to basal Na flux. However, amiloride does not completely inhibit the cAMP-stimulated Isc. In this study, the cAMP-stimulated, amiloride-insensitive Isc was characterized, using vasopressin or forskolin to raise cell cAMP. After basal Isc is inhibited by amiloride, forskolin stimulates Isc, conductance, and bidirectional 36Cl flux. Stimulation of Isc depends on the presence of both Na and Cl; stimulation of conductance depends on the presence of Cl. 36Cl flux studies showed that the cAMP-stimulated, amiloride-insensitive Isc is equivalent to net Cl flux. It is inhibited by ouabain and by furosemide or bumetanide added to the solution bathing the basal surface of the epithelium. In view of the effect of cAMP in some other epithelia, we suggest that cAMP activates apical membrane Cl channels that are in series with a Na-K-Cl cotransporter in the basolateral plasma membrane.

Amiloride↗
PubMed1986

Mechanism of central hyperglycemic effect of cholinergic agonists in fasted rats.

The influence of cholinergic agonists on central nervous system (CNS) regulation of blood sugar homeostasis was studied in fasted rats. When carbachol, muscarine, bethanechol, methacholine, or neostigmine was injected into the third cerebral ventricle, it caused a dose-dependent increase in the hepatic venous plasma glucose concentration. However, in the case of 1,1-dimethylphenyl-4-piperazinium iodide (DMPP) or nicotine, the level of hepatic venous glucose did not differ from that of the saline-treated control rats. The increase in glucose level caused by neostigmine was dose-dependently suppressed by coadministration of atropine. These facts suggest that cholinergic activation of muscarinic receptors in the CNS plays a role in increasing hepatic glucose output. Injection of neostigmine (5 X 10(-8) mol), an inhibitor of cholinesterase, into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norepinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through a femoral vein completely prevented the increase of glucagon after administration of neostigmine, although the increase of hepatic venous glucose and epinephrine levels were still observed. Neostigmine-induced increments in glucose did not occur in adrenalectomized rats. This suggests that the secreted epinephrine acts directly on the liver to increase hepatic glucose output.

Adrenalectomy↗
PubMed1986

Effect of periaqueductal morphine injection on thermal response in rats.

The effect of morphine injection into the midbrain periaqueductal gray (PAG) was examined on thermal response in rats. Rectal temperature (Tre) was recorded in unanesthetized and unrestrained animals before and after PAG morphine injection of 5 or 10 micrograms in cold (10 degrees C), neutral (22 degrees C), and hot (34 degrees C) environments. Both doses of morphine caused hyperthermia. Sixty to 105 min after the injection, Tre rose by 1.0-1.5 degrees C regardless of ambient temperature. Naloxone (2 mg/kg, i.p.) blocked the hyperthermic effects of morphine. Injection sites producing hyperthermia were distributed mostly in the ventral PAG and its ventral environs. The analgesic effect of morphine was examined by the tail-flick test. Locations of morphine injection effective for producing analgesia were restricted to the ventral area of the region responsible for hyperthermia. Magnitude of the hyperthermia did not significantly differ between animals with or without analgesia. The effect of PAG morphine (5 micrograms) was tested on tail vasomotor response to hypothalamic and scrotal thermal stimulations in urethane anesthetized (1.0 g/kg) animals. Threshold hypothalamic temperature for the vasodilation was lower at a scrotal temperature of 40 degrees C than at 30 degrees C. Following PAG morphine, threshold hypothalamic temperature rose and the difference in threshold hypothalamic temperature at the two scrotal temperatures disappeared.

Animals↗