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Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 109 records · Page 6Linked to original sources
PubMed1990

Enhanced neuroinhibitory effect of diltiazem in blood vessels of spontaneously hypertensive rats.

This study investigated the effects of diltiazem (a Ca2(+)-entry blocker) on neuromuscular junctions of blood vessels in hypertension. In isolated perfused mesenteric vasculatures prepared from spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY), the effects of diltiazem on norepinephrine release from vascular adrenergic neurons and pressor responses were examined. The influences of extracellular Ca2(+)-reduction on these responses were also studied. Stimulation evoked pressor responses and norepinephrine release were significantly greater in the mesenteric vasculatures of SHR than in those of WKY. Diltiazem inhibited both pressor responses and norepinephrine release during electrical nerve stimulation in a dose-dependent manner. The suppression of these responses was more pronounced in SHR than in WKY. Reduction of extracellular Ca2(+)-concentration also decreased the responses in SHR and WKY, and the inhibitory degree was significantly greater in SHR than in WKY. These results demonstrate that diltiazem affected the presynaptic site of the mesenteric vasculatures and decreased the stimulation-evoked norepinephrine release from vascular adrenergic neurons with a concomitant reduction of pressor responses of the preparation. Furthermore, the marked inhibition of pressor responses and norepinephrine release by diltiazem or Ca2(+)-depletion in SHR may suggest the increased Ca2(+)-dependency in vascular neurotransmission in this model of hypertension.

Animals↗
PubMed1990

Contribution of calmodulin and protein kinase C to renin release in spontaneously hypertensive rats.

This study was designed to evaluate the contribution of calmodulin and protein kinase C to renin release from isolated glomeruli of spontaneously hypertensive rats (SHR, Okamoto and Aoki). Male 7-week-old SHR and age-matched control Wistar-Kyoto rats (WKY) were used in this study. Isolated glomeruli were sealed in the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 mL/min. Renin release was increased by calmodulin inhibitor, W-7, and protein kinase C inhibitor, H-7, in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 and lower maximal levels by H-7 compared to WKY. These results indicate that calmodulin and protein kinase C play inhibitory roles in renin release from juxtaglomerular cells. The calmodulin-mediated suppression mechanism in renin release appears to be augmented in the SHR, whereas the protein kinase C-mediated system is attenuated.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Responses of cytosolic free calcium to ADP in platelets of spontaneously hypertensive rats.

Abnormalities of Ca2+ handling have been reported in patients with essential hypertension and in spontaneously hypertensive rats (SHR). In this study, responses of cytosolic Ca2+ to ADP in platelets of SHR were examined. Four- and seven-week-old male SHR and age- and sex-matched Wistar-Kyoto rats (WKY) were used. Basal levels of the intracellular Ca2+ concentration in platelets and responses to ADP were estimated using fluorescent indicator fura-2 in the medium containing 1 mmol/L CaCl2 and Ca2(+)-free buffer with 1 mmol/L EGTA. Basal levels of platelet cytosolic Ca2+ of SHR were significantly higher than those of WKY at 4 and 7 weeks of age in the presence of external Ca2+. However, no significant difference was observed in basal levels of platelet cytosolic Ca2+ in the Ca2(+)-free EGTA-containing buffer between SHR and WKY. The peak cytosolic Ca2+ concentration evoked by ADP was significantly diminished in SHR compared with WKY in the absence of external Ca2+, whereas the responses of platelet cytosolic Ca2+ to ADP were similar in SHR and WKY in the presence of external Ca2+. These results suggest that release from intracellular Ca2+ store is reduced in SHR and that the regulation of cytosolic Ca2+ in SHR is more dependent on extracellular Ca2+ compared with WKY.

Animals↗
PubMed1990

Age-related changes in membrane fluidity of erythrocytes in essential hypertension.

In the present study, age- and calcium-related changes in the membrane fluidity of erythrocytes were examined in patients with essential hypertension by use of electron spin resonance method (ESR). The erythrocytes were obtained from patients with essential hypertension. We examined the ESR spectra for a fatty acid spin label agent (5-nitroxy stearate) incorporated into the erythrocyte membranes. The values of outer hyperfine splitting and order parameter (S) were significantly higher in subjects with essential hypertension than in the normotensive subjects. This finding indicates that the membrane fluidity of erythrocytes was lower in essential hypertension. Calcium-loading of erythrocytes with the Ca-ionophore A23187 decreased the membrane fluidity (S value was increased) more strongly in essential hypertension than in the normotensive subjects. Furthermore, this Ca-induced change in membrane fluidity was significantly correlated with age in essential hypertension. These results demonstrate that the membrane fluidity of erythrocytes is markedly decreased by calcium, especially in essential hypertension in older patients. This suggests an increased calcium-sensitivity of cell membranes in the aged hypertensive patient.

Aging↗
PubMed1990

Norepinephrine release and neuropeptide Y in medulla oblongata of spontaneously hypertensive rats.

Neuropeptide Y is colocalized with norepinephrine in both central and peripheral noradrenergic neurons. In this study, we examined the regulatory mechanisms of neuropeptide Y on norepinephrine release in the medulla oblongata of rats. Neuropeptide Y inhibited the stimulation-evoked [3H]norepinephrine release in a dose-dependent manner in slices of medulla oblongata of Sprague-Dawley rats (1 Hz, S2/S1 ratio, control, 0.946 +/- 0.040 [+/- SEM], n = 6; neuropeptide Y 1 x 10(-8) M, 0.676 +/- 0.022, n = 6, p less than 0.05; neuropeptide Y 1 x 10(-7) M, 0.589 +/- 0.014, n = 6, p less than 0.05). Neuropeptide Y potentiated inhibition of [3H]norepinephrine release by the alpha 2-agonists UK 14,304 and clonidine. The blockade of alpha 2-adrenergic receptors by RX 781,094 diminished inhibitory effects of neuropeptide Y on norepinephrine release. Pretreatment of pertussis toxin (a toxin that interferes with the coupling of inhibitory receptors to adenylate cyclase) attenuated the suppression of norepinephrine release by neuropeptide Y. In spontaneously hypertensive rats, the inhibitory effect of UK 14,304 and neuropeptide Y on norepinephrine release from the medulla oblongata was significantly less than in age-matched Wistar-Kyoto rats. These results show that neuropeptide Y inhibits norepinephrine release partially mediated by alpha 2-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins in rat medulla oblongata. Furthermore, less suppression of norepinephrine release by UK 14,304 and neuropeptide Y in spontaneously hypertensive rats suggests that alpha 2-adrenergic receptors and neuropeptide Y might be involved in the regulation of central sympathetic tone in hypertension.

Adenylate Cyclase Toxin↗
PubMed1990

Platelet noradrenaline content as an integrated measure of variations in plasma noradrenaline.

To determine whether or not platelet noradrenaline (NA) content reflects a long-term variation of plasma NA concentration, the following experiments were carried out. During a 2-hour intravenous infusion of NA in rabbits, plasma NA concentration increased rapidly to an almost consistent level 1 h later, but platelet NA content increased linearly. One hour after the infusion, the plasma NA concentration returned to normal level, while platelet NA content decreased little and only returned to the original level about 80 h later. By the 24-hour cold exposure stimulation (4 +/- 0.5 degrees C), platelet NA content and urinary NA excretion increased significantly in rats. There was a significant correlation between the urinary NA excretion and platelet NA content. In a patient with pheochromocytoma, the high plasma NA concentration returned to nearly normal levels a few hours after removal of the tumor, platelet NA content returned to normal levels 4 days after surgery. These results indicate that the measurement of platelet NA content serves as a better index for obtaining an average variation of NA concentration and sympathetic nerve activity. The measurement of platelet NA content also provides a reliable means of diagnosing pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1990

Regression of left ventricular hypertrophy in hypertensive patients: responses to exercise by antihypertensive treatment.

The effects of various antihypertensive treatments on the echocardiographic and electrocardiographic findings of left ventricular (LV) hypertrophy were studied in 75 patients with essential hypertension. The hemodynamic effects of the therapy during exercise were also compared. LV mass by echocardiogram was significantly reduced by beta-blockade and angiotensin converting enzyme inhibition (ACEI), but only slightly reduced by Ca channel blockade. QRS high voltage criteria of LV hypertrophy by electrocardiogram were reduced by all 3 of these antihypertensive treatments. At submaximal exercise, the pressor responses were attenuated by captopril, but not influenced by metoprolol or nifedipine. The increase in plasma norepinephrine by exercise was significantly suppressed after captopril, but was somewhat augmented after metoprolol or nifedipine. These observations indicate that the responses of hemodynamics and sympathetic nervous activity to exercise are different after the treatment by beta-blocker, Ca channel blocker or ACEI, in spite of the equal antihypertensive effect. However, it is suggested that the regression of LV hypertrophy might be induced by antihypertensive therapy, though the different grade by the individual drug.

Adrenergic beta-Antagonists↗
PubMed1990

Effects of a calcium-antagonist on vascular sympathetic nerve activity in salt-dependent hypertension.

The purpose of the present study was to investigate the effects of a Ca2(+)-antagonist on vascular sympathetic nerve activity in salt-dependent hypertension. Isolated mesenteric vasculature preparations from reduced renal mass-salt hypertensive and age-matched normotensive control rats were used to examine the effects of diltiazem on vascular responsiveness and norepinephrine release from sympathetic nerve endings. Pressor responses and endogenous norepinephrine release during electrical nerve stimulation were significantly greater in preparations from salt-dependent hypertensive rats than from normotensive control rats. Diltiazem inhibited both stimulation-evoked pressor responses and norepinephrine release in a dose-dependent manner. The attenuation of these responses was more pronounced in preparations from rats with salt-dependent hypertension than in those from control rats. These results indicate that norepinephrine release from vascular adrenergic neurons is enhanced in the mesenteric vasculatures of rats with salt-dependent hypertension. The marked reduction of stimulation-evoked pressor responses and norepinephrine release by diltiazem suggests that enhanced Ca2(+)-dependent adrenergic transmission may contribute to the exaggerated vascular sympathetic tone in salt-dependent hypertension.

Analysis of Variance↗
PubMed1990

Clinical studies on the occurrence and the pathogenesis of optociliary veins.

We reviewed retrospectively 20 cases of optociliary vein over the past 5 years. Fifteen of the 20 cases (75%) were over 40 years of age. There was no sex differences (9 males and 11 females). Causative ocular diseases were: central retinal vein occlusion (14 cases, 70%); optic disc drusen (2 cases, 10%); and optic nerve sheath meningioma, high myopia, glaucoma, congenital anomaly (1 case each, total 20%). The number of patients with an optociliary vein was high in central retinal vein occlusion (14/190 cases, 7.4%). We concluded that occurrence of optociliary vein is not restricted to cases with optic nerve sheath meningioma and this shunt vessel may occur under other conditions in which central retinal venous return is seriously disturbed. The most common cause of optociliary vein is central retinal vein occlusion.

Adolescent↗
PubMed1990

Effects of a protein kinase C inhibitor (H-7) on norepinephrine release from vascular adrenergic neurons in spontaneously hypertensive rats.

This study was performed to investigate the effects of a specific protein kinase C inhibitor (H-7) on vascular adrenergic transmission in hypertension. In the isolated mesenteric vasculature of spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY), we have examined the effects of H-7 on norepinephrine (NE) release from vascular adrenergic neurons. Endogenous NE release during periarterial nerve stimulation was inhibited by H-7 in a dose-dependent manner with a concomitant reduction of pressor responses of the preparation. The inhibition of NE release was not affected by an uptake blocker of NE (desipramine). In SHR, the stimulation-evoked NE release and pressor responses were significantly greater than in age-matched WKY. The suppressive magnitude of stimulation-evoked NE release and pressor responses by H-7 were pronounced in SHR compared with WKY. These results demonstrate that endogenous NE release and pressor responses were increased in the mesenteric vasculature of SHR. Furthermore, the marked inhibition of NE release and pressor responses by H-7 in SHR may suggest the presence of enhanced protein kinase C-dependent regulation of vascular adrenergic transmission, which may contribute to the calcium-related abnormalities in this form of hypertension.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

[Effects of calcium antagonists or beta-blockade on left ventricular diastolic function in essential hypertension].

This study was performed to assess the effect of a calcium channel blocker (nifedipine) and beta-blockade (atenolol) on left ventricular early diastolic function and filling in essential hypertension (WHO stage I, II; HT). Twenty-two untreated patients were randomly divided as nifedipine (11 patients) and atenolol (11 patients) treatment groups and both the groups had complete echocardiographic and Doppler studies. Twenty normotensive cases served as controls. Clinical and echo-Doppler data obtained at baseline and four weeks after initiation of each therapy showed no difference between the two HT groups as to mean blood pressure (before therapy, 119 +/- 3 vs 117 +/- 11 mmHg; after therapy, 106 +/- 3 vs 110 +/- 3 mmHg), left ventricular dimension, left atrial dimension, and wall thickness. To evaluate early diastolic function, the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and that from MVO to the O point of the apexcardiogram were measured. The IIA-O interval was also calculated. The peak velocities in the rapid filling (R) and atrial contraction phases (A) were measured using pulsed Doppler echocardiography at the center of the mitral orifice. The MVO-O/IIA-MVO and A/R ratios were also calculated. Compared with the controls, the IIA-O interval (143.9 +/- 6.8 msec) and the IIA-MVO interval (81.5 +/- 4.9 msec) were significantly prolonged in HT (p less than 0.01). There was no significant difference between the MVO-O interval and R. Velocity A (54.2 +/- 2.7 cm/sec) and the A/R ratio (1.01 +/- 0.11) increased significantly in HT (p less than 0.05). The IIA-O interval (before therapy, 153.3 +/- 7.6 vs after therapy, 134.3 +/- 6.2 msec) and IIA-MVO interval (87.3 +/- 6.3 vs 77.8 +/- 5.9 msec) decreased and R (43.7 +/- 3.8 vs 49.1 +/- 3.0 cm/sec) increased significantly with nifedipine. The IIA-O interval (135.7 +/- 11.3 vs 150.4 +/- 7.6 msec) and the MVO-O (58.4 +/- 3.9 vs 66.5 +/- 4.7 msec) interval were significantly prolonged with atenolol, however the IIA-MVO interval, R, and A/R did not change. A (57.5 +/- 4.0 vs 50.2 +/- 2.9 cm/sec) was also significantly decreased with atenolol. There was a significant correlation between reduction in velocity A and prolongation in the MVO-O interval (r = -0.62, p less than 0.05) with atenolol. These results suggested that the prolongation of the diastolic closure rate of the mitral valve by atenolol was related to increased ventricular filling and decreased atrial contraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

[Magnetic resonance imaging of coronary artery lesions using modified spin-echo sequence].

Magnetic resonance imaging of the cardiovascular system has been beset with difficulties in obtaining clear images due to prominent artifacts which course in the direction of the phase encoding axis. These artifacts are commonly believed to derive from blood flow. However, in the ECG-gated spin-echo (SE) sequence using two-dimensional Fourier transform reconstruction, variation in effective repetition time due to physiological changes in the R-R interval of ECG may also result in prominent artifacts. To eliminate these artifacts, we developed a new method, the modified spin-echo (MSE) sequence, by adding a nonselective 90 degree radio-frequency pulse and an optional delay time (Td) prior to the conventional SE sequence. In the MSE sequence, artifacts derived from the cardiovascular system were markedly suppressed. Using the MSE sequence, we attempted direct imaging of the coronary vessels, and obtained very clear images of the coronary arteries and veins. Organic lesions in the coronary arteries were also clearly imaged, including coronary stenosis, dilatation, coronary fistulae, and abnormality of the origin of the right coronary artery. The MSE sequence may offer a clinical advantage in obtaining coronary artery images, and may be used to evaluate coronary artery disease.

Arteries↗
PubMed1989

Greater calmodulin-dependent regulation of neurotransmitter release and vascular responsiveness in chronic Doca-salt hypertension.

The present study was carried out to investigate the role of calmodulin in the adrenergic transmission of deoxycorticosterone acetate (DOCA)-salt hypertension. In perfused mesenteric vasculatures prepared from DOCA-salt hypertensive rats (seven to eight weeks after operation) and age-matched normotensive control rats, the effects of a specific calmodulin antagonist (W-7: N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide) on the norepinephrine release and vascular responsiveness were examined. Endogenous norepinephrine overflow during electrical nerve stimulation was significantly greater in the mesenteric vasculatures of DOCA-salt hypertensive rats both at low (5 Hz) and high (15 Hz) frequencies than in those of the normotensive controls. Vasoconstrictor responses to electrical nerve stimulation or exogenous norepinephrine were also enhanced in the DOCA-salt hypertension compared to those in the controls. The calmodulin antagonist (W-7) inhibited the stimulation-evoked norepinephrine overflow and pressor responses in a dose-dependent manner. The suppressive magnitudes in these responses by W-7 were significantly greater in the mesenteric vasculatures of the DOCA-salt hypertension than in those of the control rats. These results demonstrate that the vascular adrenergic neurotransmission might be enhanced in the mesenteric vasculatures of the DOCA-salt hypertensive rats. Further, it is suggested that the marked reduction in stimulation-evoked norepinephrine overflow and vasoconstrictor responses by W-7 showed the greater calmodulin-dependent regulation in the vascular adrenergic activity of DOCA-salt hypertension.

Animals↗
PubMed1989

Facilitatory effects of ouabain and digitalis-like substance on adrenergic transmission in hypertension.

The purpose of the present study was to examine the role of Na+,K+-ATPase activity in vascular adrenergic transmission of hypertension. In isolated perfused mesenteric vasculatures of spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, seven- to ten-weeks-old) and age-matched Wistar Kyoto rats (WKY), the effects of ouabain, a potent Na+,K+-ATPase inhibitor, or partially purified plasma obtained from salt-induced hypertension on pressor responses and norepinephrine overflow were investigated. Pressor responses and norepinephrine overflow during electrical nerve stimulation were significantly greater in SHR than in WKY. Ouabain increased the stimulation-evoked pressor responses and norepinephrine overflow. This facilitation was more prominent in SHR than in WKY. Partially purified plasma obtained from reduced renal mass-salt hypertensive rats, which had a crossimmunoreactivity with digoxin, also increased the pressor responses and norepinephrine overflow during electrical nerve stimulation, and the effects were greater in SHR than in WKY. These results suggest that Na+,K+-ATPase on vascular adrenergic neurons has an important role in the regulation of neurotransmitter release, and that its activity might be enhanced in SHR.

Animals↗
PubMed1989

A new macrolide, TE-031 (A-56268), in treatment of experimental Legionnaires' disease.

The activity of a new macrolide, TE-031 (A-56268), against Legionella pneumophila in vitro was superior to the activities of roxithromycin, erythromycin and josamycin. The tissue concentrations of TE-031 in guinea pigs after oral administration (20 mg/kg) was much higher than those of roxithromycin, erythromycin and josamycin. The maximum concentration of TE-031 was 107.0 mg/kg in the lung, and 1.4 mg/l in the serum. The uptake of macrolides by cells collected by bronchoalveolar lavage in guinea pigs was measured by a radioisotopic method. The maximum ratios of intracellular to extracellular concentration of TE-031, roxithromycin, josamycin and erythromycin were 71.9, 24.8, 39.7 and 7.9, respectively. In infected guinea pigs, with the exception of erythromycin, the ratios were reduced to approximately half the values in normal animals. TE-031 showed greater therapeutic efficacy against experimental L. pneumophila pneumonia than roxithromycin, erythromycin and josamycin. TE-031 is a promising drug for treatment of legionella pneumonia and should be investigated in a clinical study on human Legionnaires' disease.

Animals↗