Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 127 records · Page 7Linked to original sources

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

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

[Long-term prognosis related to coronary risk factors, clinical characteristics of acute myocardial infarction and coronary angiographic findings in the elderly].

In order to clarify the characteristics of acute myocardial infarction in the elderly, we investigated the clinical profile and long-term prognosis of patients with myocardial infarction in the past 13 years. The early fatality rate (within 30 days after onset) in the relatively younger patients (less than 65 years old) was 8.8%, and in the older patients (greater than 65 years old) was 29.1%. The fatality rate was significantly higher in older than in younger patients. On coronary and left ventriculography, the older patients showed multi-vessel lesions with decreased ejection fraction and cardiac index. According to the cumulative survival curves related to the coronary risk factors, no significant differences were found with or without smoking or hypertension. However, the long-term prognosis of the patients with controllable hypercholesteremia was better than in uncontrollable patients less than 65 years old. No significant difference was found in patients with hypercholesteremia over age 65. The long-term prognosis of the patients with uncontrollable diabetes mellitus was worse than that of controllable diabetic patients.

Aged↗

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

Inhibition of norepinephrine release by presynaptic alpha 2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats.

This study investigated norepinephrine release during electrical nerve stimulation and inhibitory characteristics of presynaptic alpha 2-adrenoceptors in perfused mesenteric vasculature from deoxycorticosterone acetate (DOCA)-salt hypertensive rats (7-8 weeks after surgery). Electrical stimulation of sympathetic innervation caused a significantly greater release of endogenous norepinephrine into the mesenteric vasculature of DOCA-salt hypertensive rats than in age-matched normotensive controls. Pressor responses to electrical nerve stimulation were also enhanced in DOCA-salt hypertension. Yohimbine, a potent alpha 2-adrenoceptor blocking agent, potentiated the stimulation-evoked release of norepinephrine into the vasculature in normotensive rats. This effect was blunted in DOCA-salt hypertension. These results suggest that increased norepinephrine release from the sympathetic nerve endings in DOCA-salt hypertension might partly reflect an impaired presynaptic alpha 2-adrenoceptor-mediated inhibition, which could enhance vascular sympathetic tone in this model of hypertension.

Animals↗

PubMed1989

Neurotransmitter release and vascular responsiveness in mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats.

In order to investigate the peripheral neuroeffector functions of renal hypertension, norepinephrine release from the sympathetic nerve endings and vascular responsiveness were evaluated in the mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats (2K, 1C-HT). Norepinephrine release and pressor responses during periarterial nerve stimulation (40 V, 5 msec rectangular pulses for 1 min, 5, 10 and 15 Hz) were unchanged during the acute phase (3 weeks after surgery), and were rather reduced during the chronic phase (7-8 weeks after surgery) in 2K, 1C-HT compared to sham-operated normotensive control rats. By contrast, the vasoconstrictor responses to exogenously applied norepinephrine were significantly greater in 2K, 1C-HT than in the normotensive controls. From these observations, it seems unlikely that peripheral adrenergic function in the blood vessels plays an important role in the pathogenesis of 2K, 1C-HT. However, the increased sensitivity of vascular smooth muscle cells to norepinephrine may contribute to the maintenance of high blood pressure in the face of reduced vascular sympathetic tone in this form of hypertension.

Animals↗

PubMed1989

Blood pressure and sympathetic activity following responses to aerobic exercise in patients with essential hypertension.

Fourteen untreated patients with essential hypertension (EH) were subjected to mild aerobic exercise with the intensity at 50% of the maximum oxygen uptake (VO2max) twice a week for 12 weeks, as compared with 14 normotensive subjects (NT). Blood pressure and norepinephrine (NE) in plasma, platelet and urine were measured as the indices of sympathetic activity. In EH, a significant fall in both systolic and diastolic blood pressure was observed. In addition, exercise training produced a significant decrease both urinary and platelet NE, but not in plasma NE. Neither significant changes in blood pressure nor NE in plasma, platelet and urine were observed in NT. These results suggest that an inhibition of the sympathetic nervous system might be related to the blood pressure fall in physical exercise training.

Adult↗

PubMed1989

Effects of ketanserin, verapamil and diltiazem on vascular sympathetic nerve activity in hypertension.

This study was carried out to investigate the hypotensive mechanisms of ketanserin and Ca-antagonists (verapamil and diltiazem) in hypertension. Perfused mesenteric vasculatures were prepared in spontaneously hypertensive rats (SHR, Okamoto and Aoki strain) and age-matched Wistar Kyoto rats (WKY), and the effects of these drugs on vascular responsiveness and norepinephrine release from the sympathetic nerve endings were examined. Pressor responses and endogenous norepinephrine release during periarterial nerve stimulation were significantly increased in SHR compared with age-matched WKY. Ketanserin, verapamil and diltiazem inhibited the stimulation-evoked pressor responses and norepinephrine release dose-dependently, respectively. The suppressive magnitudes of these responses by ketanserin, verapamil and diltiazem were greater in SHR than in WKY. The results demonstrate that ketanserin, verapamil and diltiazem might inhibit norepinephrine release from the vascular adrenergic neurons more strongly in hypertension. This sympatho-depressive effect may contribute, at least partially, to the hypotensive mechanisms of these antihypertensive drugs.

Animals↗

PubMed1989

[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension].

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.

Adult↗

PubMed1989

[Contribution of calmodulin to renin release in spontaneously hypertensive rats].

A comparative study was designed to evaluate the contribution of calmodulin 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 rat (WKY) were used in the present study. Glomeruli were isolated by the method of Beierwaltes et al. Isolated glomeruli were placed within the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 ml/minute at 37 degrees C. Renin release was increased by calmodulin inhibitor, W-7 in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 compared to WKY. This result indicates that calmodulin plays an inhibitory role in renin release from juxtaglomerular cells. Calmodulin-mediated suppression mechanism in renin release is augmented in SHR.

Animals↗

PubMed1989

[Contribution of hypertension to left ventricular diastolic function in patients with asymmetrical apical hypertrophy].

This study was designed to ascertain the contribution of hypertension to the early diastolic time intervals in asymmetrical apical hypertrophy (AAH). Eighteen patients with untreated AAH were categorized as those with (n = 13) and without (n = 5) hypertension. Isovolumic relaxation time and early diastolic filling were determined in four groups: normotensive subjects (n = 20), patients with essential hypertension (n = 20), AAH with hypertension, and AAH without hypertension. Early diastolic function was measured by the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and the interval from MVO to the O point of the apexcardiogram. The IIA-O interval was also calculated. Peak velocities in the rapid filling phase (R) and atrial contraction phase (A) were measured using two-dimensional Doppler echocardiography in the center of the mitral orifice in diastole. The MVO-O/IIA-MVO and A/R ratios were also calculated. 1. In the AAH with and without hypertension groups, the IIA-O, IIA-MVO, and MVO-O intervals were significantly prolonged. The IIA-O and MVO-O intervals in the AAH without hypertension group were more prolonged than were those in the AAH with hypertension group. In patients with essential hypertension, the IIA-O and the IIA-MVO intervals were prolonged, but there was no prolongation of the MVO-O interval. 2. The MVO-O/IIA-MVO ratio was lower in essential hypertension and in the AAH with hypertension groups, and significantly higher in the AAH without hypertension group. 3. There was no significant change of the R, A, and A/R in each group. These results indicated that prolonged left ventricular relaxation was distinguished in essential hypertension. In AAH with hypertension, the same prolongation was observed, but the disturbance of early diastolic filling was mild. It is suggested that apical hypertrophy has a possible association with hypertension, though it may more properly belong to cardiomyopathy.

Adult↗

PubMed1988

The role of calmodulin in neurotransmitter release and vascular responsiveness in spontaneously hypertensive rats.

This study was designed to investigate the role of calmodulin in adrenergic transmission in hypertension. In perfused mesenteric vasculature from spontaneously hypertensive rats (SHR, 7-9 weeks of age) and age-matched Wistar Kyoto rats (WKY), the effects of a specific calmodulin antagonist (W-7) on norepinephrine overflow and vascular responsiveness to endogenous and exogenous norepinephrine were examined. The vasoconstrictor responses to electrical nerve stimulation and exogenous norepinephrine as well as norepinephrine overflow during electrical nerve stimulation were significantly enhanced in SHR compared with those in age-matched WKY. The calmodulin antagonist, W-7, reduced not only vasoconstrictor responses but also norepinephrine overflow during nerve stimulation. These inhibitory effects of W-7 were significantly greater in SHR than in WKY. The results demonstrate that norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were increased in SHR. The marked reduction in norepinephrine overflow and pressor responses by W-7 might suggest the greater calmodulin-dependent adrenergic transmission in this model of hypertension.

Animals↗

PubMed1988

Effects of calcium antagonists on membrane fluidity in hypertension--an electron spin resonance study.

We examined alterations in membrane fluidity of hypertension and the effects of calcium antagonists on these changes by means of an electron spin resonance (ESR) and spin-label technique. Washed erythrocytes from spontaneously hypertensive rats (SHRs; aged 4 and 10-13 weeks) and from patients with essential hypertension, or cultured vascular smooth muscle cells from SHRs were examined and compared with those from normotensive controls. Electron spin resonance spectra for a fatty acid spin label-agent (5-nitroxy stearate) in the membranes were obtained. The values of hyperfine splitting and other parameters of the spectra were significantly higher in erythrocytes from hypertensive rats than in normotensive controls. Similar results were obtained in cultured vascular smooth muscles. These findings indicate that the membrane fluidity might be decreased in hypertension. When calcium was loaded to erythrocytes with Ca-ionophore A23187, the fluidity was decreased. The alternative degrees were greater in hypertensive rats than in controls, and these hypertensive changes were antagonized by diltiazem or verapamil. The results revealed that abnormalities of membrane fluidity in hypertension might be more prominent in the presence of calcium. Further, it is suggested that calcium antagonists could correct these membrane abnormalities in hypertension.

Adult↗

PubMed1988

Ketanserin decreases sympathetic nervous activity in hypertension.

This study was performed to investigate whether ketanserin (a serotonergic receptor antagonist) might affect the sympathetic nerve activity in resistance vessels of hypertension. Isolated perfused mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHRS, Okamoto and Aoki, 20-22 weeks old) and age-matched Wistar Kyoto rats (WKY), and effects of ketanserin on norepinephrine overflow from the adrenergic nerve endings as well as on vascular responsiveness were examined. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited by ketanserin, in a dose-dependent manner. Norepinephrine overflow during electrical nerve stimulation was also suppressed by ketanserin. Inhibitory degrees of pressor responses and norepinephrine overflow during electrical nerve stimulation by ketanserin were significantly greater in SHRs than those in WKY rats. These results suggest that ketanserin could affect presynaptic neurotransmitter release from the adrenergic nerve endings in resistance vessels. These sympatho-depressive actions might contribute, at least partially, to the hypotensive mechanisms of ketanserin.

Animals↗