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Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 145 records · Page 8Linked to original sources
PubMed1988

Relationship between the sympathetic nervous system and sodium potassium adenosine triphosphatase inhibitor in salt-sensitive patients with essential hypertension.

In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.

Blood Pressure↗
PubMed1988

Increased concentration of calcium channel and intracellular free calcium in the acute phase of deoxycorticosterone acetate salt hypertension.

Cardiac calcium channels and platelet Ca2+ concentrations were examined in deoxycorticosterone acetate (DOCA)-salt hypertension in rats to clarify the role of calcium channels in the regulation of intracellular Ca2+. Calcium channels were determined by the radioligand binding method and platelet Ca2+ concentrations were measured by a fluorescent Ca2+ indicator, Quin-2. The number of cardiac calcium channels was increased in DOCA-salt hypertension compared with controls 10 days after nephrectomy. Platelet Ca2+ concentrations were also increased in the acute phase of DOCA-salt hypertension. No significant changes were observed in the number of cardiac calcium channels and in platelet Ca2+ concentrations in the chronic phase of DOCA-salt hypertension. These results suggest that the increased platelet Ca2+ concentrations are induced by the increase in the number of calcium channels in the acute phase of hypertension.

5'-Nucleotidase↗
PubMed1988

Membrane abnormality of erythrocytes is highly dependent on salt intake and renin profile in essential hypertension: an electron spin resonance study.

The purpose of the present study was to investigate membrane fluidity in essential hypertension using electron spin resonance (ESR) and spin-labelling. Erythrocytes from patients with untreated essential hypertension were examined and compared with age-matched normotensive subjects. The values of outer hyperfine splitting (2T') and order parameter (S) of the ESR spectra for a fatty acid spin label agent (5-nitroxy stearate) were significantly higher in essential hypertension than in the normotensive subjects. However, these values were not changed in secondary hypertension. This finding indicates that the membrane fluidity of erythrocytes was lower in essential hypertension. Further, the abnormality was attenuated with low-salt intake, and, on the contrary, was more prominent with high-salt intake in essential hypertension. Calcium loading to erythrocytes in vitro caused a greater decrease in the membrane fluidity in essential hypertension than in the normotensive controls. This calcium-induced change in the membrane fluidity was significantly inversely correlated with the value of plasma renin activity in essential hypertension. These results suggest that abnormality in the membrane fluidity might be emphasized in the presence of calcium, especially in low-renin essential hypertension, implying enhanced calcium sensitivity in this type of hypertension.

Calcium↗
PubMed1988

Endogenous noradrenaline re-uptake blocking factor in rats with reduced renal mass hypertension.

This study was carried out to elucidate the involvement of the peripheral sympathetic nervous system in the pathogenesis of reduced renal mass (RRM)-salt hypertension in rats. Male Wistar rats underwent subtotal nephrectomy (70-80% reduction in renal mass). On the 10th postoperative day, systolic blood pressure was higher in RRM-salt rats than in RRM-water rats. Perfusion of isolated mesenteric vasculature from normotensive rats, with the deproteinized plasma from RRM-salt hypertensive rats induced significantly higher pressor responses and noradrenaline overflow with electrical stimulation than the perfusate from RRM-water normotensive rats; the responses to exogenous noradrenaline showed no significant changes. In the presence of desipramine, noradrenaline overflow did not increase following perfusion with plasma from RRM-salt hypertensive rats. These data indicate that plasma from rats with RRM-salt hypertension might contain some noradrenaline re-uptake blocking factor.

Animals↗
PubMed1988

Role of substance P and neurotensin in the regulation of neurosecretion and vascular responsiveness in hypertension.

The purpose of the present study was to investigate the effects of vasoactive neuropeptides, such as substance P or neurotensin, on vascular adrenergic neurotransmission in hypertension. In perfused mesenteric vasculatures prepared from spontaneously hypertensive rats (SHR), we examined the effects of substance P and neurotensin on vascular responsiveness and noradrenaline release from the sympathetic nerve endings. Stimulation-evoked noradrenaline release and pressor responses were inhibited by substance P and neurotensin. In SHR, the noradrenaline release and pressor responses during electrical nerve stimulation were significantly greater than in Wistar-Kyoto rats (WKY). The inhibitory effects of these responses by substance P and neurotensin were attenuated in SHR compared with WKY. These results showed that substance P and neurotensin could affect the presynaptic site of the blood vessels and cause a decrease in electrically stimulated noradrenaline release from the vascular adrenergic neurons. The reduction of noradrenaline release and pressor responses by substance P and neurotensin in SHR might suggest insufficient regulation of the vascular adrenergic transmission by these vasoactive peptides in hypertension.

Animals↗
PubMed1988

Protein kinase C-dependent and calmodulin-dependent regulation of neurotransmitter release and vascular responsiveness in spontaneously hypertensive rats.

This study was designed to investigate the role of protein kinase C and calmodulin in adrenergic transmission in hypertension. In isolated mesenteric vasculature prepared from spontaneously hypertensive rats (SHR, Okamoto and Aoki strain) and age-matched Wistar-Kyoto rats (WKY), we examined the effects of protein kinase C inhibitor (H-7) and calmodulin antagonist (W-7) on pressor responses and noradrenaline release from the vascular adrenergic neurons. Endogenous noradrenaline release and vasoconstrictor responses evoked by periarterial nerve stimulation were significantly enhanced in SHR compared to those in age-matched WKY. Protein kinase C inhibitor H-7 and the calmodulin antagonist W-7 inhibited the stimulation-evoked noradrenaline release and pressor responses, respectively, in a dose-dependent manner. Further, these inhibitory effects of H-7 and W-7 were greater in SHR than in WKY. These results demonstrate that noradrenaline release and vascular responsiveness are increased in the mesenteric vasculatures of SHR. The marked reduction in noradrenaline release and pressor responses induced by H-7 and W-7 in SHR suggests the presence of enhanced protein kinase C-dependent and calmodulin-dependent regulation of adrenergic neurotransmission, which may contribute to the calcium abnormalities in this model of hypertension.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Evidence in volume-dependent hypertension for an augmenting factor for norepinephrine overflow from sympathetic nerve endings.

It has been reported that salt loading induces a blood pressure rise in rats whose renal mass has been reduced. We examined the involvement of the peripheral sympathetic nervous system in the pathogenesis of hypertension in subtotally nephrectomized and salt-loaded rats. Male Wistar rats (200-240 g) underwent subtotal nephrectomy (removal of 70-80% of the renal mass). After surgery, 1% saline was given ad libitum as drinking water in the experimental group (E), while tap water was given to the controls (C). On the 10th day after nephrectomy, blood pressure was determined, and plasma samples were collected. Deproteinized plasma samples were diluted with Ringer-Locke solution (1/40 v/v), and were perfused into isolated mesenteric artery-intestinal loop preparations of normotensive male Wistar rats. Pressor responses and norepinephrine overflow induced by electrical nerve stimulation, and the pressor responses to exogenous norepinephrine were assessed before and after the addition of deproteinized plasma to the perfusate. Systolic blood pressure was significantly elevated in the experimental group (E: 150 +/- 5 mmHg, C: 109 +/- 4 mmHg, p less than 0.01). When deproteinized plasma from the experimental group was perfused, pressor responses to electrical nerve stimulation were significantly increased (E: 167.2 +/- 13.7%, C: 91.1 +/- 6.4%; p less than 0.01), as was norepinephrine overflow (E: 117.3 +/- 6.4%, C: 90.7 +/- 5.9%; p less than 0.05), while responses to exogenous norepinephrine were only slightly augmented compared with the control group (E: 120.0 +/- 2.7%, C: 105.5 +/- 9.0%; n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Membrane fluidity of erythrocytes and its relevance to renin profile in essential hypertension.

This study was performed to investigate the membrane fluidity of hypertension by means of an electron spin resonance (E.S.R.) and a spin-labeling technique. Erythrocytes from patients with untreated essential hypertension (WHO I, II) and secondary hypertension were compared with those from normotensive subjects, and E.S.R. spectra for a fatty acid spin label agent (5-nitroxy stearate) incorporated into the erythrocyte membranes were obtained. The values of outer hyperfine splitting (2T'parallel) and order parameter (S) were significantly higher in erythrocytes from patients with essential hypertension than in those from normotensive subjects. However, these values were not significantly changed in patients with secondary hypertension compared with those in the normotensive subjects. This finding may indicate the reduced erythrocyte membrane fluidity in essential hypertension. Calcium-loading to erythrocytes with calcium-ionophore caused a greater decrease in the membrane fluidity of erythrocytes in patients with essential hypertension than in those from the normotensive subjects. This Ca-induced change in membrane fluidity was inversely correlated with plasma renin activity in essential hypertension. In addition, changes in membrane fluidity by Ca-loading in essential hypertension were inhibited by Ca-antagonists (diltiazem, verapamil). These results demonstrate that the membrane fluidity of erythrocytes might be decreased in essential hypertension, and that this abnormality could be accelerated by calcium, especially in low renin essential hypertension. Furthermore, it is suggested that Ca-antagonists might correct this Ca-abnormality at cellular levels of hypertension.

Adult↗
PubMed1988

Effects of ouabain on adrenergic neurotransmission in spontaneously hypertensive rats.

The purpose of the present study is to determine the role of Na+,K+-ATPase in adrenergic neurotransmission of hypertension. Isolated perfused mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-10 weeks old) and age-matched normotensive Wistar Kyoto rats (WKY). The effects of ouabain, a Na+,K+-ATPase inhibitor, on the norepinephrine overflow from the sympathetic nerve endings were examined. Norepinephrine overflow from the nerve endings as well as pressor responses during electrical nerve stimulation were significantly greater in SHR than in WKY. Ouabain increased the norepinephrine overflow evoked by electrical nerve stimulation, even in the presence of an uptake-blocker of norepinephrine. Further, the facilitatory effect of ouabain on stimulation-induced norepinephrine overflow was more prominent in SHR than in WKY. These results suggested that ouabain-sensitive Na+,K+-ATPase on sympathetic nerve terminals could have an important role in the regulation of neurotransmitter release, and that its activity might be enhanced in SHR compared with WKY.

Animals↗
PubMed1988

Inhibitory actions of captopril on norepinephrine release from adrenergic nerve endings in spontaneously hypertensive rats.

The purpose of the present study was to investigate the mechanisms of the hypotensive actions of an angiotensin converting enzyme inhibitor of the hypotensive actions of an angiotensin converting enzyme inhibitor (captopril) in hypertension. In perfused mesenteric vasculatures from spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, 10-13 weeks of age) and age-matched normotensive Wistar Kyoto rats (WKY), the effects of captopril on vascular responsiveness and norepinephrine release from the adrenergic nerve endings were examined. The vasoconstrictor responses and norepinephrine release during the electrical nerve stimulation were significantly enhanced in SHR compared to those in age-matched WKY. Captopril reduced both vasoconstrictor responses and norepinephrine release during the electrical nerve stimulation, dose-dependently. These inhibitory effects of captopril were significantly greater in SHR than in WKY. The results demonstrate that captopril affects presynaptic sites on the resistance vessels and causes a decrease in electrically-stimulated norepinephrine release from the adrenergic nerve endings. The marked reduction of both pressor responses and norepinephrine release by captopril in SHR suggests an enhanced renin-angiotensin system in the vascular walls of hypertension.

Animals↗
PubMed1988

[Tissue characteristics in left ventricular hypertrophy using magnetic resonance imaging].

For 15 normotensive patients with asymmetric septal hypertrophy (ASH), 10 hypertensive patients with concentric hypertrophy (CH), and five normal subjects (N), we examined changes in myocardial T1 and T2 values related to the cardiac cycle. The usefulness of those values in differentiating diseases with left ventricular hypertrophy was evaluated. Left ventricular (LV) short-axis spin echo images and inversion recovery images were obtained at endsystolic and diastolic cardiac phases, and T1 and T2 images were calculated. The regional wall thickness (WT) and T1 and T2 values were measured in the anterior septum, anterior wall, lateral wall, posterior wall and posterior septum. Myocardial T1 and T2 values were significantly decreased in systole (T1: 185.6 +/- 37.9 msec, T2: 24.4 +/- 6.3 msec, mean +/- SD) compared to those in diastole (T1: 249.2 +/- 56.7 msec, T2: 31.7 +/- 9.4 msec). In both the ASH and CH groups, significant correlations were observed between diastolic T1 values and WT (ASH: r = 0.80, p less than 0.01, CH: r = 0.45, p less than 0.01), and between diastolic T2 values and WT (ASH: r = 0.58, p less than 0.01, CH: r = 0.60, p less than 0.01). In the regions where diastolic WT were more than 17 mm, T1 values in the ASH group (343.4 +/- 40.5 msec) were significantly higher than those of the CH group (247.3 +/- 21.4 msec), although the mean wall thickness values were similar in both groups. The T1/WT and T2/WT were significantly lower in the CH group than those in the ASH and N groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Single cell laser light scattering spectroscopy in a flow cell: repeated sickling of sickle red blood cells.

We performed dynamic laser light scattering measurements of hemoglobin aggregates in single, sickle erythrocytes. Sickle erythrocytes were attached to the poly-(L-lysine)-coated surface of a flow cell. They were exposed to several oxygenation-deoxygenation cycles by repeatedly changing the flowing solution. The rate of cycling was found to be a determining factor for the formation of irreversible morphologic alterations as well as irreversible hemoglobin aggregates. In slow cycling, the sickle erythrocytes took an irreversible, irregular, rounded shape, and hemoglobin aggregates were observed even in the oxygenated state after 20 cycles. In the fast cycling, however, these changes did not take place even after 60 cycles.

Anemia, Sickle Cell↗
PubMed1987

Particle motion in single acinar cells observed by microscope laser light scattering spectroscopy.

We report here the direct observation of the motion of cytoplasmic subcellular organelles and macromolecules within single, metabolically active, pancreatic acinar cells using microscope laser-light scattering spectroscopy (MLLSS). The relative amount and the "effective diffusion coefficient" of the mobile particles shows a marked difference in magnitude between the apical and basal regions of the cell. Secretory stimulation evoked by the cholinergic agonist bethanechol induces changes in the relative motion in the cytoplasm of approximately one fifth of the acinar cells. This study demonstrates the feasibility and utility of a novel technique, MLLSS, for the analysis of intracellular events in regions as small as (2 micron)3 in single, granule secreting cells. It also shows MLLSS to be a powerful tool for the detection and measurement of altered motion in discrete subcellular regions of small mammalian cells after biochemical and pharmacological manipulations.

Animals↗
PubMed1987

Electron spin resonance studies of erythrocytes from spontaneously hypertensive rats and humans with essential hypertension.

The purpose of the present study was to investigate erythrocyte membrane abnormalities in hypertension by means of an electron spin resonance and spin-label technique. The erythrocytes from spontaneously hypertensive rats (SHR) and humans with untreated essential hypertension were examined and compared with their normotensive counterparts, and electron spin resonance spectra were obtained for a fatty spin-label agent (5-nitroxy stearate) incorporated into the erythrocyte membranes. The value of outer hyperfine splitting (2T' parallel) was significantly higher in erythrocytes of SHR and humans with essential hypertension than in erythrocytes of normotensive controls (at 37 degrees C: SHR, 56.14 +/- 0.51 gauss [G], n = 8; Wistar-Kyoto rats, 52.22 +/- 0.86 G, n = 4, p less than 0.01; humans with essential hypertension, 56.94 +/- 0.27 G, n = 11; normotensive subjects, 55.44 +/- 0.36 G, n = 8, p less than 0.01). The order parameter (S) was also increased in the hypertensive rats and humans compared to their respective normotensive controls. When calcium was loaded to erythrocytes with calcium ionophore A23187 (0.9 microM) and CaCl2 (1.0 mM), the parameters of the spectra were increased. These changes were more prominent in the hypertensive groups than in the normotensive controls. These results revealed that the erythrocyte membranes of the hypertensive subjects tolerated different spin motions than those of the normotensive controls in the electron spin resonance study and that membrane fluidity might be decreased in hypertension. Additionally, calcium loading to erythrocytes caused the reduction of membrane fluidity. Therefore, it is suggested that an abnormality of calcium handling at the cellular level might affect physical properties of the biomembranes in hypertension.

Adult↗
PubMed1987

The role of epinephrine as a neuromodulator in spontaneously hypertensive rats.

The present study was carried out to elucidate the role of epinephrine as a neuromodulator in hypertension. The effects of epinephrine on norepinephrine release from the sympathetic nerve endings were examined in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). Norepinephrine overflow during electrical nerve stimulation (5, 15 Hz) was significantly greater in SHR than in WKY. Low concentration of exogenous epinephrine (5.5 X 10(-9) M) potentiated norepinephrine overflow during nerve stimulation in SHR, and this (at 15 Hz stimulation) was antagonized by propranolol (5.0 x 10(-7) M), whereas, the overflow in WKY was reduced by the same concentration of epinephrine. A higher concentration of epinephrine (1.4 x 10(-8) M) decreased norepinephrine overflow in both SHR and WKY, and this change (at 15 Hz stimulation) was antagonized by yohimbine (1.0 x 10(-7) M). Further, magnitudes of the suppressions were smaller in SHR than in WKY. These results suggest that altered modulations of norepinephrine release by epinephrine through presynaptic beta- and alpha 2-adrenoceptors might induce increased sympathetic nerve activity in SHR.

Animals↗
PubMed1987

Intracellular free calcium concentration, Ca++ channel and calmodulin level in experimental hypertension in rats.

Using fluorescent calcium indicator quin2, we studied intracellular free calcium concentration in platelets that have a number of features similar to vascular smooth muscle cells. Intracellular free calcium concentration in platelets of male SHR was significantly higher at 4, 11 and 28 weeks old compared with age-matched male WKY. However, no significant difference was observed in platelets cytosolic free calcium level of DOCA-salt hypertensive and two-kidney, one clip hypertensive rats in the chronic stage. Cardiac Ca++ channels were estimated by means of radioligand binding method with [3H]-nimodipine. No significant changes were observed in the concentration and affinity of cardiac Ca++ channel in SHR, DOCA-salt hypertensive and two-kidney, one clip hypertensive rats. Calmodulin levels in mesenteric arteries of SHR were significantly decreased in comparison with those of WKY. However no significant differences were observed in DOCA-salt hypertensive rats in the chronic stage. These results indicate that the increase in intracellular free calcium concentration of SHR is not the secondary change caused by high blood pressure. It is impossible to detect the ratio of the three states (open, resting and inactivated) of Ca++ channel. Therefore, there remains a possibility of the changes in the ratio of the states of Ca++ channel. The observed abnormalities of Ca++ regulation may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1987

Presynaptic alpha 2-adrenoceptor mediated regulation of norepinephrine release in perfused mesenteric vasculatures in young and adult spontaneously hypertensive rats.

The present study was designed to evaluate the role of the presynaptic alpha 2-adrenoceptor in the pathogenesis of hypertension. Norepinephrine overflow during sympathetic nerve stimulation and its changes by presynaptic alpha 2-adrenoceptor inhibition were examined in the perfused mesenteric vasculatures of young and adult spontaneously hypertensive rats (SHR) compared with age-matched Wistar Kyoto rats (WKY). Electrical sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from the adrenergic nerve terminals in young SHR than in age-matched WKY. Yohimbine, an alpha 2-adrenoceptor blocking agent, facilitated norepinephrine overflow from the adrenergic nerve terminals. The effects of yohimbine on norepinephrine overflow and pressor responses to electrical nerve stimulation were less in young SHR than in age-matched WKY. Norepinephrine overflow in adult SHR was similar to that in adult WKY, and differences in the effect of yohimbine on norepinephrine overflow between SHR and WKY were not marked at this chronic stage. These results suggest that enhanced norepinephrine overflow in the mesenteric vasculatures can be observed only in young SHR; this may be due in part to an impaired negative feed-back mechanism on the nerve terminals by presynaptic alpha 2-adrenoceptors.

Age Factors↗