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Biomedical subjects

E Kato

Publications and source records attributed to E Kato.

At least 91 records · Page 5Linked to original sources
PubMed1983

Acetylcholine-induced electrical responses in neuroblastoma cells.

The response to iontophoretic application of acetylcholine in the mouse neuroblastoma cell line N1E-115 was composed of three phases. The initial fast depolarizing phase was blocked by 10 microM d-tubocurarine, but not by 0.1 microM atropine. This phase was followed by a transient hyperpolarization which in turn was followed by a secondary slow depolarization. Both the hyperpolarization and slow depolarization were blocked by atropine (0.1 microM), but not by d-tubocurarine (10 microM). The hyperpolarization and slow depolarization were also evoked by iontophoretic application of the muscarinic agonist methacholine. Under voltage-clamp conditions, an initial fast inward current, a transient outward current, and a secondary slow inward current were recorded in response to acetylcholine application. These three phases of current correspond to the three phases of the membrane potential response. The initial fast inward current increased in amplitude by hyperpolarization of the membrane, and decreased by depolarization. The mean reversal potential was estimated to be -1 mV. The outward current increased in amplitude by depolarization, decreased by hyperpolarization, and reversed its polarity at -67 mV. Alteration of external K+ concentration shifted the reversal potential in the manner expected for an increase in potassium permeability. The slow inward current increased in amplitude by hyperpolarization, decreased by depolarization, and reversed its polarity at +20 mV. It is concluded that the initial fast inward current is mediated by a nicotinic receptor similar to that in muscle end-plate membranes and in postsynaptic membranes of the sympathetic ganglia. Both the outward current and the slow inward current are mediated by muscarinic receptors. The outward current results from an increase in the membrane permeability to K+, and the slow current appears to be carried, at least in part, by Na+.

Acetylcholine↗
PubMed1982

Long-term hemodialysis in a patient with primary amyloidosis, renal failure, and a vascular necrosis of the femoral heads.

A 38-year-old woman had polyarthralgia, proteinuria, and intractable diarrhea. Biopsy of the synovium, and intractable diarrhea. Biopsy of the synovium, rectal mucosa, and kidney revealed abundant deposition of amyloid, and the diagnosis of primary amyloidosis was made. The joint symptoms and diarrhea subsequently subsided, but her renal function progressively deteriorated. Maintenance hemodialysis was started 3 1/2 years later and was successfully continued for five years without major complications except for osteonecrosis of the femoral heads. Her Brescia shunt, however, failed frequently until a polytetraflouroethylene shunt was installed. Although the prognosis of primary amyloidosis and renal failure is poor, our case illustrates that persistent remission of the extrarenal symptoms can take place and that these patients can be successfully maintained by hemodialysis.

Adult↗
PubMed1982

Characteristics of the electrical response to dopamine in neuroblastoma cells.

1. The characteristics of the electrical response to dopamine in the mouse neuroblastoma cell line N1E-115 were studied. 2. Neuroblastoma cells responded to ionophoretically applied dopamine by generating a transient depolarization. Under voltage-clamp conditions, a transient inward current was recorded in response to dopamine application. 3. The receptor was more effectively activated by dopamine than by noradrenaline. Haloperidol blocked the dopamine-induced current with an apparent dissociation constant of 40 nM. Phentolamine was much less potent than haloperidol, and propranolol had no effect. 4. The dopamine-induced current was increased in amplitude by hyperpolarizing the membrane, decreased by depolarization, and reversed its polarity at + 14 mV. 5. When the external sodium concentration was decreased from 125 to 94 mM, the reversal potential was shifted in the direction of hyperpolarization by 10 mV. 6. Increasing the external potassium concentration from 0.2 to 20 mM caused a shift of the reversal potential by 13 mV in the direction of depolarization. 7. Replacement of external chloride with isethionate or glutamate caused little or no shift in the reversal potential, but increased the amplitude of the current. 8. Increase in external calcium concentration caused a block of the dopamine-induced current with an apparent dissociation constant of 1.3 mM, without altering its reversal potential. 9. It is concluded that the ionic channel activated by dopamine undergoes a conductance increase to both sodium and potassium but not to chloride or calcium.

Animals↗
PubMed1982

Effects of methylmercury on electrical responses of neuroblastoma cells.

The effects of methylmercury on a variety of electrophysiological properties of the N1E-115 neuroblastoma cells were studied using microelectrode and voltage clamp techniques. The action potential was reduced in amplitude with an apparent dissociation constant of the order of 20 microM in the face of relatively small membrane depolarization. Voltage clamp experiments revealed that both peak sodium current and steady-state potassium current were suppressed by 20-60 microM methylmercury, with a stronger effect on the sodium current than on the potassium current. The protein reagents dithiodipyridine and N-ethylmaleimide suppressed both currents. Acetylcholine receptor/channel complexes are vulnerable to the action of methylmercury; the nicotinic fast depolarizing response, the muscarinic hyperpolarizing response, and the muscarinic slow depolarizing response, were all suppressed by 10-30 microM methylmercury. In contrast, the dopamine induced response was not affected by methylmercury at 30 microM. It was concluded that methylmercury impairs both sodium and potassium channel gating mechanisms and suppresses acetylcholine receptor/channel complexes. It remains to be seen whether the effect of chronic exposure is similar to that seen after acute and high level exposure in the present study.

Acetylcholine↗
PubMed1982

[Antihypertensive and diuretic effects of indapamide in normotensive and hypertensive rats (author's transl)].

Antihypertensive and diuretic actions of indapamide (SE-1520) were investigated in rats and compared with those of trichlormethiazide (TCMT). In normotensive rats, indapamide in a dose of 100 mg/kg p.o. did not show a significant effect on the blood pressure. In DOCA-saline and uni-nephrectomized DOCA-saline hypertensive rats, indapamide above 1 mg/kg and TCMT above 3 mg/kg with single oral or repetitive administration for 2 weeks reduced the blood pressure level. In spontaneously hypertensive rats (SHR), both indapamide and TCMT lowered the blood pressure with single doses above 10 mg/kg or repetitive doses above 3 and 10 mg/kg, respectively. In the diuretic test using normal rats, indapamide in doses ranging from 0.1 to 30 mg/kg increased urine volume and urinary electrolyte excretion. TCMT showed a more potent diuretic action at a lower dose level. In SHR, indapamide and TCMT produced a greater urine volume and electrolytes excretion. Indapamide inhibited the carbonic anhydrase activity and the potency was about 1/25 of that of acetazolamide in vitro. The antihypertensive activity of indapamide was more potent than that of TCMT and the reverse order to that of their diuretic potencies. It is suggested that the mechanism of antihypertensive effect of indapamide is different from that of TCMT.

Animals↗