Biomedical subjects

M Naka

Publications and source records attributed to M Naka.

At least 37 records · Page 2Linked to original sources

PubMed1997

Occurrence of sustained increase in QT dispersion following exercise in patients with residual myocardial ischemia after healing of anterior wall myocardial infarction.

Our objective was to evaluate the effect of exercise on QT dispersion over the next 3 hours, as seen on a standard 12-lead electrocardiogram in patients with healed myocardial infarction with or without residual ischemia. We measured QT and QTc dispersion before, immediately after, and 1 and 2 hours after symptom-limited, dynamic treadmill exercise tests in 28 patients with healed anterior wall myocardial infarction with (group I, n = 18) and without (group II, n = 10) residual ischemia. The same protocol was followed in 5 group I patients after successful performance of coronary angioplasty. QT and QTc dispersion did not change immediately after exercise in group II. These parameters increased in group I (QT dispersion at rest [mean +/- SD] 57 +/- 22 ms, and after exercise 87 +/- 27 ms; QTc dispersion at rest 62 +/- 25 ms, and after exercise 114 +/- 36 ms). The increases in QT and QTc dispersion were sustained for at least 2 hours. After a successful coronary angioplasty in 5 patients, these parameters no longer increased with exercise. Thus, QT dispersion increased for at least 2 hours after exercise in patients who had residual ischemia after healing of myocardial infarction. Data obtained in 5 of these patients after coronary angioplasty support the idea that residual ischemia plays a key role in the sustained increase in QT dispersion after exercise.

Aged↗

PubMed1997

Propiverine hydrochloride, an anti-pollakiuric agent, inhibits the activity of actomyosin ATPase from the urinary bladder.

The present study was performed to investigate the effects of propiverine hydrochloride (1-methyl-4-piperidyl diphenylpropoxyacetate hydrochloride, P-4), a novel anti-pollakiuric agent, on the contractile proteins of smooth muscle. P-4 (30-300 microM) inhibited the activity of native actomyosin adenosine triphosphatase (ATPase) that had been freshly purified from canine urinary bladder, and calmodulin at 10 microM overcame this inhibition. P-4 also inhibited myosin light chain kinase from smooth muscle in a dose-dependent manner. However, at 300 microM, P-4 was unable to inhibit by 50% the activity of trypsin-treated myosin light chain kinase, which was independent of Ca2+/calmodulin. 1 mol of calmodulin bound 4 to 5 mol of [14C]P-4 in a Ca2+-dependent manner with a K(d) of 77.4 microM. These results indicate that calmodulin is one of the intracellular target molecules for P-4 and that inhibition of the action of calmodulin by P-4 might cause the inhibition of actomyosin ATPase activity, with subsequent relaxation of the smooth muscle of the urinary bladder.

Animals↗

PubMed1997

[Recovery process from myocardial stunning after transient ischemia: assessment with pulsed wave Doppler transmitral flow pattern].

Sustained left ventricular systolic dysfunction after transient myocardial ischemia is well known as "myocardial stunning", but little is known about the recovery in left ventricular diastolic function. Changes in left ventricular systolic and diastolic performance following dobutamine-induced ischemia were investigated in 13 patients with chest pain syndrome and normal coronary arteries (control) and 34 patients with coronary artery disease. Two-dimensional echocardiography and pulsed wave Doppler transmitral flow velocity curves were recorded at baseline, after infusion of a peak dose of dobutamine and at 20 min and 2 hours after dobutamine infusion. In control subjects, left ventricular ejection fraction and the peak early diastolic filling velocity increased at the peak dose of dobutamine. At 20 min after the cessation of dobutamine infusion, these values were restored to the baseline levels. In patients with coronary artery disease, ejection fraction and peak velocity increased at the peak dose of dobutamine but decreased at 20 min after infusion compared with baseline values despite the restoration of heart rate and blood pressure. Although ejection fraction increased at 2 hours compared with 20 min after infusion, peak velocity did not increase. Left ventricular diastolic dysfunction may be sustained longer than systolic dysfunction after transient myocardial ischemia.

Aged↗

PubMed1996

Decreased baroreflex sensitivity in patients with stable coronary artery disease is correlated with the severity of coronary narrowing.

Although studies have shown that arterial baroreflex sensitivity (BRS) is decreased in patients with acute myocardial infarction, BRS changes in patients with stable coronary artery disease (CAD) have not been studied extensively. We assessed BRS by the phenylephrine method in 55 normotensive and nondiabetic patients with chronic effort angina, old myocardial infarction, or both. The control group consisted of 24 age-matched patients without coronary lesions. To identify factors that determine BRS in stable CAD, we performed multivariate analysis using age, sex, left ventricular ejection fraction, pulmonary artery wedge pressure, resting systolic blood pressure, resting heart rate, the number of stenotic coronary arteries, history of myocardial infarction, and the presence or absence of angina pectoris as variables. BRS was significantly lower in patients with CAD than in control subjects (5.9 +/- 2.9 vs 6.9 +/- 2.4 ms/mm Hg, p < 0.05). In patients with CAD, BRS was inversely correlated with age, the resting heart rate, and the number of stenotic coronary vessels (p < 0.001, p < 0.005, and p < 0.005, respectively), but was independent of other clinical parameters, including the history of myocardial infarction. In control subjects, BRS was significantly correlated only with age. These results indicate that BRS is decreased in patients with stable CAD, and this decrease is correlated with the extent and severity of coronary narrowing.

Age Factors↗

PubMed1996

Novel specific chemtactic receptor for S100L protein on guinea pig eosinophils.

We isolated a new chemotactic protein from bovine lung, and its partial protein sequence analysis indicated that this protein was identical with S100L, one member of the Ca2+-binding S100 protein family. The chemotactic activity of S100L on guinea pig eosinophils is observed at 0.1nM protein concentration, and the effects appear mediated by a novel specific surface receptor. We characterized the receptor for S100L on guinea pig eosinophils. Scatchard analyses of the data that [125I]S100L bound to S100L receptor indicate the presence of two receptor populations on eosinophils with a Kd value of 3.3 x 10(-11)M and 1.1 x 10(-9)M. Thus, S100L protein has the most potent chemotactic activity on guinea pig eosinophils of all the chemotactic proteins.

Animals↗

PubMed1995

A calponin peptide enhances Ca2+ sensitivity of smooth muscle contraction without affecting myosin light chain phosphorylation.

In permeabilized smooth muscle, exogenously applied calponin binds to myofibrils and reduces Ca(2+)-activated tension (Itoh, T., Suzuki, S., Suzuki, A., Nakamura, F., Naka, M., and Tanaka, T. (1994) Pflügers Arch. Eur. J. Physiol. 427, 301-308). A calponin peptide (calponin Phe173-Arg185), which inhibits the binding of calponin to actin, blocks the action of calponin and enhances the contraction induced by submaximal Ca2+ in permeabilized vascular smooth muscle. Unlike calmodulin, this peptide enhances the Ca(2+)-induced contraction without a corresponding increase in the level of myosin light chain phosphorylation. These results suggest that calponin decreases the sensitivity of smooth muscle to Ca2+ at a given level of myosin light chain phosphorylation.

Actins↗

PubMed1995

Protein kinase C-independent activation of Raf-1 and mitogen-activated protein kinase by leukotriene B4 in guinea pig eosinophils.

Leukotriene B4 (LTB4) and phorbol 12-myristate 13-acetate (PMA) were found to activate serine/threonine kinase c-Raf-1 (Raf-1) and mitogen-activated protein (MAP) kinase in guinea pig eosinophils. Raf-1 was activated by both compounds in a time- and dose-dependent fashion, and the activation by each paralleled that of MAP kinase. The LTB4 receptor antagonist ONO-4057 prevented the LTB4-induced activation of Raf-1 and MAP kinase, but had no effect on the PMA-induced activation of these kinases. The protein kinase C (PKC) inhibitors, (+/-)1-O-hexadecyl-2-O-methylglycerol (AMG-C16) and bisindolylmaleimide (GF 109203X), suppressed the PMA-induced activation of Raf-1 and MAP kinase, but not the LTB4-induced activation of both kinases. Our findings suggest that the activation of Raf-1 and MAP kinase by LTB4 involves a PKC-independent pathway.

Animals↗

PubMed1995

Phosphorylation of calponin mediated by protein kinase C in association with contraction in porcine coronary artery.

Calponin is an actin-associated regulatory protein in smooth muscle. We report that both endothelin-1 (ET-1) and phorbol 12, 13-dibutyrate (PDBu) caused a significant increase in phosphorylation of calponin during contraction of porcine coronary artery, while high levels of KCl were ineffective. This phosphorylation was predominantly catalyzed by activation of protein kinase C(PKC). In addition, the level of phosphorylation of calponin increased closely in association with the size of the contractile force induced by PDBu. Thus, the phosphorylation of calponin in vivo by PKC might modulate in part the contraction of smooth muscle that occurs in response to ET-1 or PDBu.

Animals↗

PubMed1995

Increased receptor-mediated phospholipase D activation and Ca2+ mobilization in peritoneal polymorphonuclear leukocytes from streptozotocin-induced diabetic rats.

Phospholipase D activation was investigated in peritoneal polymorphonuclear leukocytes from streptozotocin-induced diabetic rats. Stimulation of the cells with formyl-Met-Leu-Phe resulted in a time- and dose-dependent increase in phosphatidylethanol in the presence of ethanol, and this lipid formation in cells prepared from diabetic rats was enhanced as compared to that in the case of nondiabetic rats. Furthermore, the increase in the intracellular Ca2+ concentration was also enhanced in the stimulated cells from diabetic rats. Under the present conditions, N-acetyl-beta-glucosaminidase release and superoxide generation, which are known to be dependent on phospholipase D activation, were higher in the cells from diabetic rats than those in the cells from control rats. However, there was no difference in the dissociation constant and the number of binding sites for formyl-Met-Leu-Phe between the cells from diabetic and control rats. Phosphatidylethanol formation, N-acetyl-beta-glucosaminidase release and superoxide generation in response to ionomycin or 4 beta-phorbol 12-myristate 13-acetate were not enhanced in diabetic rat cells, as compared with those in control rat cells. These results suggest that receptor-mediated phospholipase D activation and Ca2+ mobilization are enhanced in diabetic rat polymorphonuclear leukocytes, which might be due to acceleration of receptor-mediated signaling.

Acetylglucosaminidase↗

PubMed1995

Stimulation of platelet-activating factor synthesis in polymorphonuclear leukocytes from streptozotocin-induced diabetic rats.

The platelet-activating factor (PAF)-synthesizing capacity was investigated and compared in peritoneal polymorphonuclear leukocytes (PMN) from streptozotocin-induced diabetic and normal rats. PAF synthesis was significantly enhanced in the PMN from diabetic rats compared with that from normal rats stimulated with fMLP. This was manifested as the increased incorporation of [3H]acetate into PAF. Selected ion monitoring/GC/MS analysis revealed that the molecular species of PAF synthesized were mostly of the 1-hexadecyl type, and the amount synthesized in fMLP-stimulated diabetic rat PMN was 1.5 times higher than that in normal rat PMN. The fMLP-induced arachidonic acid liberation resulting from phospholipase A2 activation, was facilitated with a concomitant increase in the cytosolic Ca2+ concentration in diabetic rat PMN. The CoA-independent transacylase activity was similar in both PMN lysates, whereas acetyl-CoA:lyso-PAF acetyltransferase activity was accelerated in the diabetic rat PMN lysate. These results revealed that diabetic rat PMN has more ability to synthesize PAF, presumably due to the large increase in activated phospholipase A2 and acetyltransferase, as well as the increased cytosolic Ca2+ concentration.

Acetates↗

PubMed1995

Contribution of atrial reservoir function to ventricular filling in hypertensive patients. Effects of nifedipine administration.

We designed this study to access the importance of left atrial function as a contributor to mitral flow velocity pattern in hypertensive patients. In hypertensive patients the early diastolic flow velocity and ratio of early to late diastolic flow velocity in the mitral flow velocity pattern increase in association with sublingual administration of nifedipine. These changes have been interpreted as signs of improved left ventricular diastolic function; however, the mitral flow velocity pattern is also affected by various other factors. Thus, the nifedipine-induced changes may not necessarily indicate the improvement of left ventricular diastolic function. Transthoracic Doppler echocardiographic parameters of mitral and pulmonary venous flow velocity patterns and left ventricular M-mode echograms were obtained in 16 untreated hypertensive patients before and after sublingual administration of nifedipine (10 mg). Normal values of the parameters were determined in 50 age-matched healthy subjects. After nifedipine peak early diastolic mitral flow velocity increased beyond the normal value, although the peak increasing rate of left ventricular inner dimension, another index of left ventricular diastolic function, did not recover to the normal value. Peak systolic velocity in the pulmonary venous flow velocity pattern increased beyond the normal value, indicating improvement of the reservoir function to the left atrium during systole. Nifedipine-induced normalization of the mitral flow velocity pattern was associated with further abnormalities of the pulmonary venous flow velocity pattern, indicating enhanced left atrial reservoir function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Vasospastic angina pectoris associated with apical hypertrophic cardiomyopathy.

As the chest symptoms and electrocardiographic changes of hypertrophic cardiomyopathy are occasionally very similar to those of angina pectoris, there are some difficulties in the diagnosis and treatment of cases of ischemic heart disease associated with hypertrophic cardiomyopathy. Here we report a case of vasospastic angina pectoris associated with hypertrophic cardiomyopathy diagnosed by coronary spasm provocation test performed by intracoronary administration of acetylcholine. In the treatment of such cases, beta blockers, which have the effect of decreasing the oxygen demand of the heart and the potential to induce coronary spasm, must be administered carefully.

Acetylcholine↗

PubMed1995

The effect of repeated writing on memory.

Repeated writing, or rehearsal by writing, is a common memory strategy for the Japanese, especially when learning new logographic characters. The to-be-remembered items are written down not as external prompts, as with reminder notes, but to be memorized in the course of writing them down over and over again. In this study, we investigated whether the strategy was effective, and if so, in which condition. Experiment 1 showed that repeated writing improved memory for graphic designs but not for Chinese characters, words, or syllables. Experiment 2 showed that the effect occurred for both Japanese and American subjects, suggesting that it was not the result of a cultural background associated with a logographic language. Instead, the effect seemed to be accounted for by the encoding specificity of visual-motor information, because repeated writing improved free recall--that included writing--but did not improve recognition (Experiment 3). In Experiment 4, the strategy was applied to learning the Arabic alphabet. Finally, similarities between repeated writing and Type 1 rehearsal are discussed.

Adult↗

PubMed1994

Characterization of the myosin-binding subunit of smooth muscle myosin phosphatase.

A myosin phosphatase was purified from chicken gizzard smooth muscle. The holoenzyme is a trimer and consists of 130,000-, 38,000-, and 20,000-Da subunits (in agreement with the results of Alessi et al.: Alessi, D., MacDougall, L. K., Sola, M. M., Ikebe, M., and Cohen, P. (1992) Eur. J. Biochem. 210, 1023-1035). The catalytic subunit, 38,000 Da, is the type 1 delta isoform, and its derived amino acid sequence is identical to the rat isoform. The larger subunit bound to myosin and also interacted with the catalytic subunit. cDNA clones encoding the large subunit were isolated from chicken gizzard cDNA libraries. Overlapping clones indicated the presence of two isoforms, and open reading frames of 2889 and 3012 bases were obtained. These encoded proteins of 963 and 1004 amino acids, with masses of 106,700 and 111,600 Da, respectively. The insert in the larger isoform is in the center of the molecule, at residues 512-552. The N-terminal third of the molecule is composed of eight repeat sequences, similar to the cdc10/SWI6 or ankyrin repeat. Myosin binding and binding to the catalytic subunit are properties of a 58,000-Da fragment that represents the N-terminal part of the molecule.

Amino Acid Sequence↗

PubMed1994

Purification and characterization of a novel calcium-binding protein, S100C, from porcine heart.

A novel Ca(2+)-binding protein, which we have named S100C (Ohta et al. (1991) FEBS Lett. 295, 93-96), was purified to homogeneity from porcine heart by Ca(2+)-dependent dye-affinity chromatography. S100C possesses some properties of S100 proteins, such as self-association and exposure of a hydrophobic site upon binding of Ca2+ but it differs from S100 proteins in forms of its isoelectric point (pI = 6.2), cross-reactivity with antibodies, staining by Stains-all, and its Ca(2+)-dependent interaction with the immobilized dye. S100C bound to cytoskeletal components at physiological concentrations of Ca2+. Moreover, it was found that 125I-labeled S100C interacted with annexin I in a Ca(2+)-dependent manner. S100C also inhibited the phosphorylation of annexin I by protein kinase C. These data suggest that S100C might act to regulate the cytoskeleton in a Ca(2+)-dependent manner via interactions with annexin I.

Animals↗

PubMed1994

Effects of exogenously applied calponin on Ca(2+)-regulated force in skinned smooth muscle of the rabbit mesenteric artery.

To help elucidate the physiological role of calponin (a thin-filament-linked regulatory protein) in smooth muscle contraction, the effects of its exogenous application were investigated on actin-activated MgAT-Pase activity in crude actomyosin from chicken gizzard, and on contraction induced by Ca(2+)-dependent and -independent means in arterial smooth muscle strips skinned by saponin or beta-escin. Calponin concentration dependently inhibited actin-activated MgATPase activity with a proportional increase in its binding to actomyosin and also attenuated Ca(2+)-induced contractions, in the presence or absence of calmodulin, in skinned arterial strips. Calponin, when phosphorylated by protein kinase C, reduced both its ability to bind to actomyosin and its inhibitory action on actomyosin MgATPase. The phosphorylated calponin also had no effect on the maximum Ca(2+)-induced contraction in skinned smooth muscle, suggesting that these actions of calponin are not nonspecific. Calponin attenuated the Ca(2+)-independent contraction observed in myosin light chain thio-phosphorylated strips, or on application of trypsin-treated myosin light chain kinase. However, calponin had no effect on maintained rigor contraction. These results suggest that in vascular smooth muscle, calponin may play a physiological role in the inhibition of Ca(2+)-regulated force, possibly through a direct action on active actin-myosin interactions.

Adenosine Triphosphate↗

PubMed1994

Long-term clinical effect of nilvadipine in patients with chronic heart failure: a double-blind placebo-controlled study.

The long-term effect of calcium channel blockers on chronic heart failure is disappointing, probably because of reflex sympathetic activation through arterial vasodilation. However, nilvadipine may be beneficial for treatment of chronic heart failure since this drug has minimal effects on sympathetic activation. In this study, the effects of 12-week administration of nilvadipine or placebo on symptoms of heart failure and cardiac function were investigated in 23 patients with mild-to-moderate chronic heart failure in a double-blind trial. The patients were randomly assigned to either a nilvadipine group (16 mg daily) or a placebo group. Intergroup comparisons did not show significant differences in any parameters. Serious adverse effects were not observed during the study. Thus, this study failed to show any beneficial effect of nilvadipine in the long-term treatment of patients with chronic heart failure. We conclude that the long-term administration of nilvadipine (16 mg daily) is neither effective nor harmful in the treatment of patients with chronic heart failure.

Calcium Channel Blockers↗

PubMed1994

Effect of successful angioplasty following thrombolysis on infarct size and left ventricular function.

The role of the angioplasty following thrombolysis in acute myocardial infarction has been discussed in several studies, however the effect of successful angioplasty on infarct size and left ventricular function has not been properly evaluated. Successful reperfusion was achieved in 79 out of 104 patients with primary anterior acute myocardial infarction. These patients were classified as follows, according to the type of intervention during the acute phase: 50 patients in which thrombolysis was successful (the thrombolysis group); 12 patients who underwent successful immediate angioplasty following successful thrombolysis (the immediate angioplasty group); and 17 patients in which rescue angioplasty was successful (the rescue angioplasty group). The 25 patients whose infarct-related vessels were not reperfused after intervention were classified as the non-reperfused group. Infarct size, evaluated as defect volume by T1-201 SPECT, 1 month after the onset, was 840 +/- 154 units (mean +/- S.D.) in the immediate angioplasty group and was similar to that in the thrombolysis group (948 +/- 88 units), but significantly smaller than in the non-reperfused group (1759 +/- 108 units). There were no significant differences in left ventricular function in the immediate angioplasty group and the thrombolysis group. Successful rescue angioplasty did not have any beneficial effect on left ventricular functions or infarct size, when compared with the failed thrombolytic group (1105 +/- 169 units vs. 1617 +/- 169 units). End-diastolic volume (52 +/- 3 ml/m2) in the successful rescue angioplasty group, however, was significantly smaller than in the failed thrombolysis group (67 +/- 3 ml/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗