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Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 181 records · Page 10Linked to original sources
PubMed1986

Peripheral neural mechanism of hypertension in rat models--peripheral sympathetic neurotransmission in hypertension.

To investigate the peripheral neural mechanism of hypertension, norepinephrine release from sympathetic nerve endings was evaluated in various hypertensive rat models. The isolated mesenteric vasculatures were prepared in 7-9-week-old and 20-22-week-old spontaneously hypertensive rats (SHR), DOCA-salt hypertensive rats (DOCA-HT), two-kidney, one clip renal hypertensive rats (2K1C-HT) and their age-matched normotensive controls. The vasoconstrictor responses to exogenous norepinephrine (EN) were significantly enhanced in all hypertensive rat models compared with their age-matched normotensive controls. The pressor responses to electrical nerve stimulation (NS) were greater in SHR than age-matched Wistar-Kyoto (WKY) rats, and were also increased in DOCA-HT. The norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in the normotensive controls. In 2K1C-HT, the norepinephrine overflow by NS was somewhat reduced compared with sham-operated normotensive controls. Inhibition by calcium-antagonist (verapamil) of the pressor responses and norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in their controls. The facilitatory effect on the norepinephrine overflow exerted by the alpha 2-adrenoceptor antagonist, yohimbine, during NS was significantly less in young SHR and chronic DOCA-HT.

Animals↗
PubMed1986

[The pattern of left ventricular hypertrophy in hypertension and its relation to the hemodynamic and sympathetic responses to exercise].

A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.

Adult↗
PubMed1986

Effects of alpha-human atrial natriuretic peptides on neurosecretion and vascular responsiveness in spontaneously hypertensive rats.

Effects of alpha-human atrial natriuretic peptides (alpha-hANP) on the norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were investigated in the perfused mesenteric intestinal loop preparations from 7- to 9-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited by alpha-hANP (3.4 X 10(-7) to 1.0 X 10(-6) mol/l), and norepinephrine overflow during the nerve stimulation was concomitantly suppressed by alpha-hANP. The pressor responses and norepinephrine overflow by nerve stimulation were greater in SHR than the age-matched WKY, while the inhibition of these responses by alpha-hANP was significantly less in SHR than in WKY. These results demonstrate that alpha-hANP could affect both pre- and post-synaptic sites of the resistance vessels, and less reduction in the pressor responses and norepinephrine overflow by alpha-hANP in SHR suggests insufficient regulation of adrenergic neurotransmission by cardiac peptide in hypertension.

Animals↗
PubMed1986

Effects of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in hypertension.

The purpose of the present study was to analyse the regulatory mechanisms of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in the resistance vessels in hypertension. The perfused mesenteric arteries were used for the experiment in spontaneously hypertensive rats (SHR; 7-10 weeks old) and age-matched normotensive Wistar-Kyoto (WKY) rats. Norepinephrine overflow during electrical nerve stimulation was significantly greater in SHR than in WKY rats. A low concentration of epinephrine (5.5 X 10(-9) mol/l) potentiated norepinephrine overflow from the nerve endings in SHR, and this was antagonized by propranolol, while this overflow was reduced by the same concentration of epinephrine in WKY rats. Higher concentrations of epinephrine decreased the norepinephrine overflow both in SHR and WKY rats, and this was antagonized by yohimbine. Dopamine reduced the norepinephrine overflow during electrical nerve stimulation, suppression being significantly less in SHR than in WKY rats. These results suggest that in SHR the increased norepinephrine overflow from sympathetic nerve endings may be partly caused by the facilitatory effect of epinephrine (through presynaptic beta-adrenoceptors) and impaired dopamine-mediated inhibition on the nerve terminals, which might contribute to the enhanced adrenergic activity in hypertension.

Animals↗
PubMed1985

Microscope laser light scattering spectroscopy of single biological cells.

A microscope laser light scattering setup was developed, allowing us to do intensity autocorrelation spectroscopy on the light scattered from a volume as small as (2 micron)3. This non-invasive technique makes cytoplasmic studies possible inside single live biological cells. The effect of osmotic swelling and shrinking on the diffusion coefficient of hemoglobin inside intact red blood cells is shown as an illustrative example of the applicability and sensitivity of this new experimental method.

Erythrocyte Membrane↗
PubMed1985

Plasma noradrenaline and its deaminated metabolites in essential hypertension and pheochromocytoma.

Dihydroxyphenylglycol (DOPEG) is a metabolite of noradrenaline (NA) in the sympathetic nerve endings, and dihydroxymandelic acid (DOMA) is one in the extraneuronal tissues. The measurement of plasma DOPEG and DOMA were evaluated with NA as one of the clinical indices of sympathetic nerve activity. These were measured in essential hypertension and also applied for diagnosis of pheochromocytoma. Plasma DOPEG levels were correlated with NA. Plasma NA and DOPEG were decreased after oral administration of clonidine (150 micrograms) and plasma DOPEG levels were slowly increased after standing. Therefore, plasma DOPEG seemed to be useful as one of the rather stable indices of the sympathetic nerve activity. Plasma NA and DOPEG levels in WHO stage I essential hypertension were higher than those in normotensive controls. Observed normal plasma noradrenaline and DOPEG levels in stage II reflect the normalized sympathetic tone in this stage. The elevation of plasma NA and DOMA levels in stage III seemed to be at least partly explained by renal function disturbance. In patients with pheochromocytoma, despite of the marked elevation of plasma NA and DOMA, plasma DOPEG showed only three-fold elevation and the ratio DOPEG/NA was reduced. The simultaneous measurement of plasma NA, DOPEG and DOMA is useful to evaluate sympathetic nerve activity in essential hypertension and to differentiate pheochromocytoma in hypertension.

Adrenal Gland Neoplasms↗
PubMed1985

Effects of diltiazem (a calcium antagonist) on neurosecretion and vascular responsiveness in hypertension.

The purpose of the present study was to analyse the mechanisms of the vasodepressive action of diltiazem (one of the Ca antagonists) in hypertension. The perfused mesenteric preparation was used in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and age-matched Wistar-Kyoto rats (WKY). The effects of diltiazem on norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were investigated. Pressor responses to electrical nerve stimulation were inhibited dose-dependently by diltiazem. Norepinephrine overflow during periarterial nerve stimulation was also inhibited by diltiazem, and its suppression was significantly greater in SHR than in the age-matched WKY rats. Vasoconstrictor responses to exogenous norepinephrine were also reduced by diltiazem in both SHR and WKY rats. The inhibitory effects of diltiazem were more evident in SHR than in WKY rats. These results demonstrate that diltiazem could affect both pre- and postsynaptic sites of the resistance vessels and cause a decrease in electrically stimulated norepinephrine overflow from the sympathetic nerve endings, in addition to the direct effects on the responsiveness of the vascular smooth muscles. The marked reduction of the pressor responses and norepinephrine overflow by diltiazem in SHR might explain the Ca-dependency in the pathogenesis of hypertension.

Animals↗
PubMed1985

[The role of hypertension in apical hypertrophy].

Recent advances in echocardiography have revealed that hypertension causes several types of cardiac hypertrophy. We classified hypertensive patients by type of cardiac hypertrophy, and evaluated left ventricular function and the severity of hypertension. The subjects consisted of 257 hypertensive patients, 13 patients with cardiac hypertrophy, and 95 normotensive controls. The hypertensives were classified in four groups: no hypertrophy, concentric hypertrophy, asymmetrical septal hypertrophy (ASH), and asymmetrical apical hypertrophy (AAH). The normotensive patients with cardiac hypertrophy included nine with ASH and four with AAH. Cardiac functions in these patients were determined by echocardiography, RI-angiocardiography and cardiac catheterization. The results were as follows: Among 257 hypertensive patients, the incidence of concentric hypertrophy, ASH, and AAH was 53%, 10%, and 4%, respectively. In patients with AAH and hypertension, the hypertensive blood pressure levels and hypertensive organ involvements were mild. The blood pressures of most of these patients fell to the normal range after admission. The cardiac index and left ventricular systolic function (FS, mVCF, and ejection fraction) were significantly higher in AAH with hypertension than in the other hypertensive groups or in the normotensive controls. The hypertensive patients showed lower E-F slopes and higher A/E ratios than the normotensive controls, as well as the normotensive patients with ASH or AAH. Cardiac function did not differ appreciably between normotensive AAH and hypertensive AAH. Left ventricular dimension and left ventricular end-diastolic volume index were larger in AAH with hypertension. The total peripheral resistance of the hypertensive AAH was significantly lower than that of the hypertensives with concentric hypertrophy (p less than 0.01), though it was higher than that of the normotensive AAH (p less than 0.01). It was, therefore, concluded that mild hypertension observed in patients with AAH may be the result of regulatory mechanisms in the hyperkinetic states.

Adolescent↗
PubMed1984

In vivo observation of lens protein diffusivity in normal and X-irradiated rabbit lenses.

Using the techniques of quasielastic light scattering spectroscopy we have studied in vivo the effect of X-irradiation on the diffusivity of lens proteins as a function of position in the lens and time after irradiation. The findings were compared with those for normal lenses in vivo. The experimentally observed correlation functions show marked changes in the protein diffusivity well before substantial biochemical changes take place.

Animals↗
PubMed1984

Direct observation of delta-crystallin accumulation by laser light-scattering spectroscopy in the chicken embryo lens.

By using the technique of laser light-scattering spectroscopy, direct observation has been made on the intracellular accumulation of a crystallin protein within the cells of chicken embryo lens during the process of development. Appearance of delta-crystallin has been detected as early as day 4, and its concentration reaches a plateau at day 19. The measurements constitute a noninvasive determination of accumulation of protein molecules that specifically characterize the process of cell differentiation.

Animals↗
PubMed1984

Neurotransmitter release and vascular reactivity in spontaneously hypertensive rats.

This study was designed to investigate neurotransmitter release during the sympathetic nerve stimulation of perfused mesenteric arterial beds of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) at young and adult ages. The role of Ca in neurotransmitter release and vascular responsiveness was also examined by using a Ca-antagonist (verapamil). Pressor responses to electrical nerve stimulation and exogenous noradrenaline were greater in SHR than in WKY. Noradrenaline overflow by electrical nerve stimulation from mesenteric arterial beds was also significantly greater in young SHR than age-matched WKY. However, in adult SHR, the noradrenaline overflow was reduced compared with WKY. After verapamil infusion (5.0 X 10(-7)M approximately 2.5 X 10(-6)M), suppression of the pressor responses and noradrenaline overflow evoked by electrical nerve stimulation was greater in SHR than in WKY at both ages. The pressor responses to exogenous noradrenaline were also inhibited by verapamil more in young SHR than in young WKY. In adult SHR, the inhibition was similar to age-matched WKY. These results suggest that noradrenaline release from sympathetic nerve endings in SHR increase at a young age and decreases in adults, and depends at least partly on Ca-influx at both ages as dose vasoconstrictor reactivity. Therefore, Ca-dependency in SHR at both pre- and post-synaptic sites of neurotransmission may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1984

Increased osmotic fragility of erythrocytes in essential hypertension.

The correlation between hypertension and the osmotic fragility of erythrocytes was examined. High osmotic fragility of erythrocytes was observed in patients with essential hypertension and normotensive subjects with family history of hypertension, compared with normotensive controls without family history of hypertension. In patients with secondary hypertension, the osmotic fragility of erythrocytes was not significantly different from that of normotensive controls without family history of hypertension. The membrane fragility had no correlation with the level of blood pressure or dietary salt intake. Thus, the osmotic fragility of erythrocytes might reflect functional or structural abnormalities of cell membranes, and could be one of the genetic markers of the hypertensive predisposition.

Adult↗
PubMed1984

Alteration of presynaptic alpha 2-mediated inhibition of norepinephrine release in perfused mesenteric arteries of young and adult spontaneously hypertensive rats.

The present study was designed to evaluate norepinephrine release during sympathetic nerve stimulation and its inhibitory characteristics by presynaptic alpha 2-adrenoceptor in the perfused mesenteric arteries of young and old spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto rats (WKY). Sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from adrenergic nerve terminals in young SHR than age-matched WKY. Yohimbine, alpha 2-adrenoceptor antagonist, exerted a facilitatory effect on norepinephrine overflow from mesenteric vasculature. This effect was less in young SHR than in aged-matched WKY. On the other hand, in adult SHR the amount of norepinephrine overflow was somewhat reduced compared with age-matched WKY. The difference of the facilitatory effect on norepinephrine overflow by yohimbine between SHR and WKY was not so marked as that observed in young age. These results indicate that increased norepinephrine release from sympathetic nerve endings in young SHR could depend at least partly on impaired presynaptic alpha 2-mediated inhibition, while normal or reduced norepinephrine release in adult SHR might be an adaptive mechanism to prevent further increase in blood pressure in SHR.

Aging↗
PubMed1984

Neurotransmitter release, vascular responsiveness and their calcium-mediated regulation in perfused mesenteric preparation of spontaneously hypertensive rats and DOCA-salt hypertension.

To investigate the role of norepinephrine release from the sympathetic nerve endings and vascular responsiveness to endogenous and exogenous norepinephrine in the pathogenesis of hypertension, the perfused mesenteric preparations from spontaneously hypertensive rats (SHR) and DOCA-salt hypertension were used. In addition, the effects of two calcium antagonists on norepinephrine release by electrical stimulation and the vasoconstrictor responses to norepinephrine were examined to evaluate the calcium dependency of norepinephrine release and the vascular responsiveness in hypertension. The vascular responsiveness was increased in SHR and DOCA-salt hypertension in both early and later phases. Norepinephrine overflow from the sympathetic nerve terminals was enhanced only in young SHR and the chronic phase of DOCA-salt hypertension. After infusion of verapamil, a calcium antagonist, into the perfusate, the pressor responses and norepinephrine overflow by electrical stimulation were more inhibited in SHR, especially in young SHR, and the chronic phase of DOCA-salt hypertension than in controls. These results suggest that calcium dependency in both pre- and postsynaptic sites of neurotransmission may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1983

Hemoglobin aggregation in single red blood cells of sickle cell anemia.

A laser light scattering technique was used to observe the extent of hemoglobin aggregation in solitary red blood cells of sickle cell anemia. Hemoglobin aggregation was confirmed in deoxygenated cells. The light scattering technique can also be applied to cytoplasmic studies of any biological cell.

Anemia, Sickle Cell↗
PubMed1983

Changes in renal alpha 2-adrenoceptor in experimental hypertension in rats.

alpha 2-Adrenoceptors were studied in renal membrane fractions from spontaneously hypertensive (SHR), two-kidney, one clip hypertensive (2K, 1C HT) and DOCA-salt hypertensive (DOCA-salt HT) rats, using radioligand binding method. alpha 2-Adrenoceptor concentration in the kidney measured by [3H]yohimbine binding was significantly increased in SHR at 4 weeks old (41.5 +/- 2.8 fmol/mg protein, mean +/- SEM, p less than 0.01), 12 weeks old (54.9 +/- 2.5 fmol/mg protein, p less than 0.01) and 35 weeks old (59.8 +/- 3.4 fmol/mg protein, p less than 0.01) as compared with age-matched Wistar-Kyoto rats (WKY, 31.5 +/- 2.5, 40.9 +/- 1.8, 47.8 +/- 2.0 fmol/mg protein, respectively). There were no significant differences in binding affinity and 5'-nucleotidase activity (plasma membrane marker enzyme) between SHR and WKY at any age. In 2K, 1C HT rats, alpha 2-adrenoceptor concentration in the clipped kidney was higher than that of control rats, but alpha 2-adrenoceptor concentration in the unclipped kidney was unchanged. Binding affinity and 5'-nucleotidase activity showed no significant changes in renal hypertensive rats. In DOCA-salt HT rats, no significant change was found in concentration and affinity of renal alpha 2-adrenoceptor. The observed increase in renal alpha 2-adrenoceptor concentration in SHR may contribute to the pathogenesis and maintenance of hypertension through increased sodium and water reabsorption in the kidney.

Animals↗