Biomedical subjects

I Katoh

Publications and source records attributed to I Katoh.

At least 37 records · Page 2Linked to original sources

PubMed1997

Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

In the present study, we examined the effect of atrial natriuretic peptide (ANP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Rat ANP(1-28) stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-8) M to 10(-6) M). The 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. In addition, rat ANP(1-28) caused 22Na+ influx into the cells. The 45Ca2+ efflux was also stimulated by C-type natriuretic peptide-22 (CNP-22), but not by rat brain natriuretic peptide-45 (BNP-45). It was also observed that both rat ANP(1-28) and CNP-22 stimulated guanosine 3',5'-cyclic monophosphate production within the cells. These results indicate that ANP stimulates Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange, and that the stimulatory effect of ANP on Ca2+ efflux may be mediated via the natriuretic peptide receptor which has been shown to couple to guanylate cyclase. Since it is reported that Na+/Ca2+ exchange is important in calcium homeostasis within cells, ANP may play a role in the extrusion of intracellular Ca2+ from isolated adult rat cardiomyocytes.

Animals↗

PubMed1997

Neuropeptide Y as a stimulator of Na+ -dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

Several physiological stimuli cause a rise in intracellular Ca2+ concentration ([Ca2+]i) in cardiomyocytes. This increased [Ca2+]i must be restored to physiological resting level to ensure response to further stimuli. In the present study, we examined the effect of neuropeptide Y (NPY), which is secreted from certain adrenergic or nonadrenergic neurons, on Ca2+ efflux from freshly isolated, quiescent adult rat cardiomyocytes. The isolated cardiomyocytes were preloaded with 45CaCl2 for 1 h. Then, the fractional release of 45Ca2+ from the cells was measured. NPY stimulated the efflux of 45Ca2+ from isolated adult rat cardiomyocytes in a concentration-dependent manner (10(-8) M to 10(-6) M). NPY (10(-6) M)-induced Ca2+ efflux was 2.0 +/- 0.16% of the total cellular content. The 45Ca2+ efflux from the cells was also stimulated by Y1 receptor agonist, [Leu31, Pro34]NPY, but not by Y2 receptor agonist, NPY13-36. The effect of NPY was inhibited by a peptide NPY inhibitor, NPY18-36 and a non-peptide NPY inhibitor, benextramine to a similar extent. From these results, it is conceivable that the effect of NPY on Ca2+ efflux from cardiomyocytes is mediated through Y1 receptors. It was also observed that NPY caused a rise in [Ca2+]i to almost 150 nM. NPY-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, NPY caused a 22Na+ influx into the cells of about 1.6-fold over the basal value which was inhibited by amiloride and 5-(N,N-dimethyl)-amiloride, known Na+/Ca2+ exchange inhibitors. In addition, isoproterenol also caused 45Ca2+ efflux from the cells and which was enhanced by the addition of NPY. These results suggest that NPY stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane Y1 receptors with which NPY may couple during Na+/Ca2+ exchange.

Adenosine Triphosphatases↗

PubMed1997

Effect of docarpamine, a novel orally active dopamine prodrug, on the formation of free and sulfoconjugated dopamine in patients who underwent cardiac surgery.

To evaluate the clinical efficacy of orally active dopamine prodrug, docarpamine [N-(N-acetyl-L-methionyl)-O,O-bis (ethoxycarbonyl) dopamine], we examined its effect on the formation of free and sulfoconjugated dopamine in patients who underwent cardiac surgery. The preoperative values of free and sulfoconjugated dopamine in patients were 216 +/- 52 pg/ml and 4,930 +/- 820 pg/ml, respectively. The plasma level of free dopamine increased to 95.3 +/- 28.3 ng/ml by dopamine infusion after the operation and was sustained at a high level (87.7 +/- 26.5 ng/ml) by concomitant administration of docarpamine in spite of tapering of dopamine infusion. After stopping dopamine infusion, plasma level of free dopamine was 24.5 +/- 17.6 ng/ml maintained by oral administration of docarpamine alone. From these results, docarpamine may be a useful alternative to intravenous dopamine after cardiac surgery. Sulfoconjugated dopamine in plasma increased to 267 +/- 120 ng/ml after the start of dopamine infusion and increased further after oral docarpamine administration to 2,060 +/- 610 ng/ml. Since sulfoconjugated dopamine is thought to be a possible precursor of active free dopamine in plasma, orally administered docarpamine might be stored as a reserve pool for free dopamine in patients who undergo cardiac surgery.

Administration, Oral↗

PubMed1997

Extracellular adenosine 5'-triphosphate induces Ca2+ efflux from freshly isolated adult rat cardiomyocytes: possible involvement of Na+/Ca2+ exchange mechanism.

In the present study, we examined the effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. ATP at 1 mM caused a release of 3.6+/-0.08% of the total cellular content. The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate) (ATP-gamma s), alpha, beta-methylene-ATP and adenosine 5'-diphosphate (ADP), but not by adenosine 5'-monophosphate (AMP) or adenosine. The effect of ATP was inhibited by a known purinergic P2-receptor antagonist, but not by a P1-receptor antagonist. From these results, it is conceivable that the effect of ATP on Ca2+ efflux from cardiomyocytes is mediated through P2-purinoceptors. It was also observed that ATP caused a rise in [Ca2+]i to almost 200 nM. The ATP-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, ATP caused a 22Na+ influx into the cells of about 2.0-fold over the basal value. These result suggest that ATP stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane P2-purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine Triphosphate↗

PubMed1996

Angiotensin II as a stimulator of Na(+)-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

In cardiac tissues, angiotensin II causes inotropic and chronotropic effects on the heart. It is indicated that the mechanism of the inotropic effect of angiotensin II is attributed to an increase in cytosolic free calcium ([Ca2+]i) in cardiomyocytes. However, increased [Ca2+]i should be restored to a physiological level because cumulative elevation in [Ca2+]i leads to irreversible injury in cardiomyocytes. Whereas it is known that angiotensin II causes the increase in [Ca2+]i in cardiac cells, little is known about the mechanisms of decrease in [Ca2+]i in cardiomyocytes upon angiotensin II stimulation. In the present study, we examined the effect of angiotensin II on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Angiotensin II stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-7)-10(-5) M). The 45Ca2+ efflux from the cells was inhibited by type 1 angiotensin II receptor inhibitor. The angiotensin II-stimulated 45Ca2+ efflux was not affected by deprivation of the extracellular Ca2+, but was dependent on the presence of extracellular Na+. These results indicate that angiotensin II stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on the plasma membrane type 1 angiotensin II receptors which may couple to Na+/Ca2+ exchange.

Angiotensin II↗

PubMed1996

Effect of extracellular adenosine 5'-triphosphate on Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

The effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes was examined. ATP stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (0.01-1 mM). The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate)(ATP-gammas) and alpha,beta-methylene-ATP and adenosine 5'-diphosphate, but not by adenosine 5'-monophosphate and adenosine. The ATP-stimulated 45Ca2+ efflux was not affected by deprivation of the extracellular Ca2+, but was dependent on the presence of extracellular Na+. These results indicate that ATP stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on the plasma membrane P2 purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine↗

PubMed1996

Physiological significance of plasma sulfoconjugated dopamine in patients with hypertension--clinical and experimental studies.

Sulfoconjugated catecholamines, especially dopamine sulfate, have recently attracted much attention because of the possibility of their conversion to active free dopamine by tissue arylsulfatase. In the present study, we have measured the plasma levels of free and sulfoconjugated dopamine in patients with hypertension and have investigated the physiological significance of sulfoconjugation. Results showed that the plasma level of dopamine sulfate in patients with essential hypertension was higher than the level in control subjects, and was highest in patients with renal hypertension. However, the plasma level of free dopamine showed no significant difference between patients with hypertension and normal subjects. Moreover, after normalization of blood pressure in hypertensive patients with medication, the plasma levels of conjugated dopamine decreased to almost the control value. In the experimental study, dopamine sulfate inhibited angiotensin II-induced aldosterone release from bovine adrenal cortical cells to a similar extent as produced by free dopamine. From these results, we have concluded that plasma sulfoconjugated dopamine may regulate free dopamine in the plasma of patients with hypertension, and it may have some physiological effects on blood pressure regulation.

Adrenal Cortex↗

PubMed1996

[Surgical experience of two different types of unroofed coronary sinus].

We experienced two cases with uncommon unroofed coronary sinus. The first patient, a 55-year-old man, had a partially unroofed mid-portion of the coronary sinus. His symptoms and physical state were similar to that of atrial septal defect (ASD). Echocardiogram and angiogram revealed that the coronary sinus (CS) communicated with the left atrium (LA). We confirmed that CS had an enlarged orifice and lacked a part of its roof through the right atriotomy and the atrioseptotomy. We directly closed the defect between the LA and the CS. His postoperative course was satisfactory. The second patient, a 46-year-old man, showed mild cyanosis. He had a completely unroofed CS with left superior vena cava (LSVC), absent inferior vena cava (IVC) and hemiazygos continuity. The LSVC directly drained to the LA, and the CS was absent. A part of the posterior wall of the LA was like a groove which laid from the orifice of the LSVC to the coronary sinus ASD. The roof of this groove was covered with fibrous tissue, which was shaped like a network structure. We thought that this network was a residue of the septum between the CS and the LA. Thus we resected this structure, and reconstructed the roof by equine pericardial patch to drain the venous blood from the LSVC to the right atrium. Anomaly in the patient may be the transitional type between the completely unroofed CS and the partially unroofed CS.

Coronary Vessel Anomalies↗

PubMed1996

[Effect of amiloride on the early and late stage of postischemic recovery in isolated perfused rat hearts--possible involvement of Na+/H+ and Na+/Ca2+ exchange].

To investigate whether Na+/H+ exchange or Na+/Ca2+ exchange involves in the ischemic-reperfusion injury, we examined the effect of amiloride, a potent inhibitor of Na+/H+ exchange, on the ischemic reperfused rat heart. When, the hearts were loaded with 0.1 mM amiloride preischemically, the recovery of left ventricular developed pressure was significantly improved than that of the control group, whereas the recovery of heart rate was not influenced by amiloride pretreatment at 30 min of reperfusion. Measurement of intracellular cations revealed that intracellular Na+ accumulation in the early stage (within 5 min) of reperfusion was inhibited by amiloride pretreatment. On the other hand, in the late stage (from 5 min to 30 min) of reperfusion, Ca2+ overload was inhibited by amiloride. These results suggest that Na+/H+ exchange mainly participates in the early stage of reperfusion injury and Na+/Ca2+ exchange system, secondary to the Na+/H+ exchange, participates in the late stage of the reperfusion injury. Moreover, pretreatment with amiloride also decreased creatine phosphokinase activity in the coronary effluent and completely abolished the incidence of ventricular arrhythmia during reperfusion. It is assumed that the improvement of postischemic cardiac dysfunction induced by amiloride pretreatment may be attributable to its inhibition on the resultant Ca2+ accumulation during ischemia.

Amiloride↗

PubMed1996

[Lymphangitis].

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Acute Disease↗

PubMed1996

[Lymphedema].

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Adolescent↗

PubMed1996

Mechanism of ATP-induced Ca2+ efflux from freshly isolated adult rat cardiomyocytes: possible involvement of Na+/Ca2+ exchange.

Physiological stimulation causes a rise in intracellular Ca2+ concentration in cardiomyocytes. However, it has not yet been elucidated what mechanisms are involved in the reduction of cytosolic free Ca2+ levels, including those which underlie Ca2+ efflux from the cells. In the present study, we examined the effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+, efflux from freshly isolated adult rat cardiomyocytes. The isolated cardiomyocytes were preloaded with 45CaCl2 for one hour. Then, the fractional release of 45Ca2+ from the cells was measured consecutively. ATP stimulated the efflux of 45Ca2+ from isolated adult rat cardiomyocytes in a concentration-dependent manner (0.01-1 mM). The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate) (ATP-gamma S), alpha, beta-methylene-ATP and adenosine 5'-diphosphate (ADP), but not by adenosine 5'-monophosphate (AMP) or adenosine. The effect of ATP was inhibited by a specific purinergic P2-receptor antagonist, but not by a P1-receptor antagonist. From these results, it is conceivable that the effect of ATP on Ca2+ efflux from cardiomyocytes is mediated through P2-purinoceptors. The ATP-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, ATP caused a 22Na+ influx into the cells. These results suggest that ATP stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane P2-purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine Triphosphate↗

PubMed1996

Effect of cromakalim on ischemic and reperfused immature heart: experiments with isolated neonatal New Zealand white rabbit hearts.

To elucidate whether K+ channels are involved in the ischemia-reperfusion injury in immature heart, we examined the effect of cromakalim, a potent opener of ATP-sensitive K+ channel (KATP channel), on the ischemic and reperfused neonatal New Zealand white rabbit heart. The experiments were divided into control group and cromakalim pretreated group. When, the heart was loaded with 10 microM cromakalim preischemically, the recovery of heart rate and left ventricular developed pressure were significantly improved than those of the control group. Pretreatment with cromakalim also decreased lactate excretion in the coronary effluent. Measurements of cation contents with atomic absorption method revealed that intracellular K+ content was lower in cromakalim pretreated group at preischemia, end of ischemia and 20 min after ischemia. Intracellular accumulation of Na+ and Ca2+ at reperfusion period was inhibited by cromakalim pretreatment. From these results, it is assumed that cromakalim might act on KATP channels of plasma membrane and reduces the K+ content of the cardiomyocytes which in turn inhibits Na+ and Ca2+ accumulation during the reperfusion period. Prevention of Na+ and Ca2+ accumulation after ischemia might be a reason for cardioprotective effect of cromakalim on neonatal New Zealand white rabbit heart.

Animals↗

PubMed1995

Alterations of the cytoskeletal organization in tumor cell lines by a cardiotonic drug, vesnarinone, through protein tyrosine phosphorylation.

We describe nonspecific and moderate activation of cellular protein tyrosine phosphorylation by a chemical compound, vesnarinone, which results in enhanced synthesis and/or assembly of cytoskeletal proteins and morphological alterations in several transformed cells. In A431 cells, vesnarinone induced tyrosine phosphorylation of the overexpressed epidermal growth factor receptors (EGFR) as well as other unidentified proteins, increased the synthesis of cytokeratins, and caused amplification of the intermediate filament networks and cell flattening. The drug effects were abolished by tyrphostin, a protein tyrosine kinase inhibitor. Two other cell lines responded to the drug with increased synthesis of a cell type-specific cytoskeletal protein: vimentin in QG56 human lung carcinoma cells and alpha-tubulin in NIH3T3 cells transformed with v-src. In all cell lines tested, the drug-induced tyrosine phosphorylation was localized in cell-cell and cell-substrate contacts as detected by immunofluorescent staining. Responsive protein substrates and their sensitivity to the drug varied from one cell line to another as observed by immunoblot analysis. Vesnarinone exerted neither activating nor inhibitory effect on in vitro enzyme reactions including EGFR tyrosine kinase, v-src kinase, and protein tyrosine phosphatases. This suggests that vesnarinone indirectly activates tyrosine phosphorylation of membrane proteins related to cell adhesion, which influences a signaling pathway linked to the stress fiber assembly in certain cell lines. The possible mechanism by which vesnarinone induces the cellular responses is discussed.

3T3 Cells↗

PubMed1995

Technique for constructing the pulmonary trunk for tetralogy of Fallot with pulmonary atresia.

In expectation of the growth of a new pulmonary arterial trunk in total correction of tetralogy of Fallot with pulmonary atresia, we used pedicled autologous pericardium combined with left atrial appendage as the posterior wall of a new pulmonary arterial trunk. In cases of long discontinuity between the right ventricular infundibulum and left pulmonary artery, our technique could be recommended for early repair of tetralogy of Fallot with pulmonary atresia.

Child, Preschool↗

PubMed1995

Physiological significance of plasma sulfoconjugated dopamine: experimental and clinical studies.

Sulfoconjugated catecholamines have been regarded simply as metabolites of free catecholamines. However, a conjugated form of the catecholamine, dopamine has recently attracted much attention because it is present at high levels in the plasma of humans and experimental animals. We carried out experimental and clinical studies to determine the physiological significance of this large amount of dopamine conjugate in the plasma. Clinical studies showed that the plasma level of dopamine sulfate decreased significantly during the acute phase of heart failure, whereas that of free dopamine increased. Moreover, the plasma level of conjugated dopamine in patients with essential hypertension was higher than that in control subjects, and being highest in patients with renal hypertension. In experimental studies, we examined the activity for deconjugating DA sulfate in homogenates of organs from dogs. The kidney and liver exhibited the highest activities, and in the heart, the activity was higher in the atrium than the ventricle. We also examined the effect of dopamine sulfate on isolated perfused rat heart. Dopamine sulfate was found to be converted to free dopamine, which was responsible for the positive inotropic action, in atrial tissue. Moreover, deconjugation of DA sulfate to the free form was accelerated by a high work lord on the heart. From these results, we conclude that the formation of dopamine sulfate plays a role in regulating the level of plasma free dopamine and that plasma dopamine sulfate may be a storage or reserve form of dopamine. Free (or active) dopamine may be formed through a deconjugation reaction when necessary.

Adult↗

PubMed1994

Effects of the potassium channel openers cromakalim and pinacidil on catecholamine secretion and calcium mobilization in cultured bovine adrenal chromaffin cells.

The effects of two K+ channel openers, cromakalim and pinacidil, on voltage-dependent and receptor-mediated catecholamine secretion and Ca2+ mobilization in bovine adrenal chromaffin cells were studied to determine the role of membrane K+ channels in the regulation of a Ca(2+)-dependent secretory process. Both cromakalim and pinacidil stimulated the efflux of 86Rb (used to monitor K+ permeability) from preloaded cells. Cromakalim and pinacidil did not affect the catecholamine secretion induced by excessive depolarization with 56 mM K+, but inhibited that induced by moderate depolarization with 31 mM K+ in a concentration-dependent manner (1 microM-100 microM). The 31 mM K(+)-induced 45Ca2+ influx and increase in intracellular free Ca2+ concentration [Ca2+]i were also inhibited by these agents at similar concentrations to those for inhibition of catecholamine secretion. Cromakalim and pinacidil inhibited catecholamine secretion, 45Ca2+ influx and increase in [Ca2+]i induced by stimulation of nicotinic acetylcholine (ACh) receptors with carbamylcholine. Furthermore, both cromakalim and pinacidil inhibited the increase in [Ca2+]i induced by carbamylcholine in the absence of extracellular Ca2+, which is thought to be mediated by muscarinic ACh receptors. On the other hand, they did not affect catecholamine secretion induced by Bay-K 8644, Ba2+, A23187, histamine or bradykinin. These results indicate that the K+ channel openers, cromakalim and pinacidil, selectively inhibit catecholamine secretion induced by moderate depolarization or by nicotinic ACh receptor stimulation by inhibiting Ca2+ influx and increase in [Ca2+]i. Furthermore, the results suggest that these K+ channel openers-sensitive membrane K+ channels are involved in the regulation of catecholamine secretion mainly indirectly through effects on the voltage-dependent membrane Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1994

Quantitative evaluation of intraarterial lymphocyte injection therapy for lymph edema using MR imaging.

Five patients with unilateral leg lymph edema had intraarterial injections of lymphocytes in the affected leg with consequent improvement in 3. To assess the degree of lymph edema, T2 and intensity ratio between the 2 legs in STIR images were used. Mean and SD of T2 values in the subcutaneous tissue were measured using a triple echo sequence and found larger on the edematous side than in the opposite extremity. The mean T2 shortening obtained after the lymphocyte therapy correlated well with the reduction of limb circumference. Mean T2 reflects the fluid content, and SD of T2 the fluid distribution in the subcutaneous tissue. The degree of lymph edema and the effect of therapy can be evaluated quantitatively by measuring the value of the T2 relaxation time.

Adult↗