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Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 163 records · Page 9Linked to original sources
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↗
PubMed1987

The cause of death, risk factors and long-term prognosis of acute myocardial infarction.

Three hundred and eighty-six patients with acute myocardial infarction in the past 11 years between 1975 and 1985 were investigated retrospectively to clarify fatality, cause of death and long-term prognosis in relation to their risk factors and age. The average number of patients admitted in each year was 24.4 for the first 5 years and 44.0 cases per year in the last 5 years. The fatality decreased from 20.3% in the first 5 years to 15.7% in the last 5 years. A major cause of hospital death was cardiogenic shock and congestive heart failure. One hundred and thirty-six patients had coronary arteriography within 2 months after admission. They were divided into three groups; the young (less than or equal to 40 year old)-, middle (41-50 year old)-, and old (greater than or equal to 51-year old)-aged groups. Among the young-aged group, serum cholesterol levels at admission were significantly higher in patients with multi-vessel lesions than those in patients without multi-vessel lesions, while there were many heavy smokers who did not show a significant lesion of the coronary artery. These observations suggest that hypercholesterolemia may act as an important risk factor for coronary arteriosclerosis in young patients, and also that a heavy smoking may promote an initiation of myocardial infarction in young patients without severe coronary artery stenosis. The cumulative 5 and 10 year survival rate for all groups was 84% and 61%, respectively. Fifty-seven patients had reinfarctions, and thirty patients died. The survivors were younger and had a good tolerance to treadmill exercise test at discharge.

Age Factors↗
PubMed1987

Inhibitory action on alpha-human atrial natriuretic polypeptide on vascular adrenergic neurotransmission is attenuated in spontaneously hypertensive rats.

The purpose of the present study is twofold, firstly to investigate the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on norepinephrine overflow from sympathetic nerve endings, and secondly to compare vascular responsiveness in perfused mesenteric preparations in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and a cohort of Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, the pressor responses to electrical nerve stimulation or exogenous norepinephrine application were inhibited by alpha-hANP. Norepinephrine overflow was also suppressed by alpha-hANP, during nerve stimulation. The pressor responses and norepinephrine overflow during nerve stimulation were significantly greater in SHR than in WKY rats. The inhibitory effect of alpha-hANP on these responses was reduced in SHR. These results indicate that alpha-hANP could affect both pre- and post-synaptic sites of the resistance vessels. Further, the reduced inhibition of pressor responses and norepinephrine overflow by alpha-hANP in SHR suggests an insufficient regulation of adrenergic transmission by alpha-hANP in hypertension.

Animals↗
PubMed1987

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

This study was designed to investigate the role of calmodulin in adrenergic neurotransmission of resistance vessels. The effects of various calmodulin antagonists (trifluoperazine, W-7, calmidazolium, chlorpromazine, fluphenazine) on the vascular responsiveness and norepinephrine overflow from adrenergic nerve endings were examined in perfused rat mesenteric vasculature preparations. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited dose-dependently by each calmodulin antagonist. Norepinephrine overflow from the sympathetic nerve endings during electrical nerve stimulation was also suppressed by calmodulin antagonists. These results indicate that calmodulin antagonists affected both pre- and post-synaptic sites of adrenergic neurotransmission, suggesting that calmodulin is involved both in neurosecretion and vascular smooth muscle contractions in peripheral resistance vessels.

Animals↗
PubMed1987

Alterations in calcium-handling of erythrocytes in spontaneously hypertensive rats. Calcium-induced changes in the osmotic fragility of erythrocytes in hypertension.

To investigate the sensitivity to calcium of erythrocytes in hypertension, changes in the osmotic fragility of erythrocytes following Ca-loading were observed. Washed erythrocytes were obtained from spontaneously hypertensive rats (SHR, Okamoto and Aoki) and age-matched normotensive Wistar Kyoto rats (WKY). Treatment of erythrocytes with Ca-ionophore A23187 and Ca in the medium caused a reduction in the osmotic fragility which correlated with the Ca-concentration. The degree of alteration in the osmotic fragility of erythrocytes was greater in SHR than in WKY. Oral administration of hydralazine to SHR significantly reduced the blood pressure. However, the alterations in the osmotic fragility of erythrocytes secondary to Ca-loading were not different between hydralazine-treated and untreated SHR. In the presence of a Ca-antagonist (verapamil or diltiazem) in the medium, the reduction of the osmotic fragility of erythrocytes caused by Ca-loading was inhibited, and the differences between SHR and WKY were abolished by Ca-antagonists. These results suggest that the greater changes in osmotic fragility of erythrocytes caused by Ca-loading in SHR could be due to a genetic abnormality of Ca-handling by the cell membranes, and that this abnormality might cause an increase in intracellular Ca, which contributes, in part, to the pathogenesis of hypertension.

Animals↗
PubMed1987

Diminished prostaglandin-mediated inhibition of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats.

This study was performed to investigate prostaglandin (PG)-mediated regulation of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats (SHR). The effects of PGE2 on the pressor responses and norepinephrine overflow during the periarterial nerve stimulation were examined in the perfused mesenteric vascular beds from SHR and age-matched Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, PGE2 inhibited the overflow of norepinephrine in response to the electrical nerve stimulation. On the contrary, when indomethacin was infused into the preparations, the norepinephrine overflow induced by the nerve stimulation was increased. In SHR, the neurogenic vasoconstriction and norepinephrine overflow during the nerve stimulation were significantly greater than in WKY. PGE2 in the medium inhibited the pressor responses and norepinephrine overflow during the nerve stimulation dose-dependently in WKY, while the inhibitory effects of PGE2 in SHR were blunted. These results suggest that PGE2 is an important hormone in regulating sympathetic vascular tone and that presynaptic inhibition of vascular adrenergic transmission by PGE2 is attenuated in SHR.

Animals↗
PubMed1987

Effects of captopril on neurosecretion and vascular responsiveness in hypertension.

The purpose of the present study was to investigate the mechanisms of hypotensive action of an angiotensin converting enzyme inhibitor (captopril) in hypertension. In perfused mesenteric vasculatures from spontaneously hypertensive rats (SHR) and normotensive Wistar kyoto rats (WKY), the effects of captopril on the vascular responsiveness and norepinephrine overflow from the adrenergic nerve endings were examined. The vasoconstrictor responses and norepinephrine overflow during the electrical nerve stimulation was significantly enhanced in SHR compared with WKY. Captopril reduced not only vasoconstrictor responses but also norepinephrine overflow during the nerve stimulation in a dose-dependent fashion. The suppressions of these responses by captopril were significantly greater in SHR than in WKY. These results demonstrate that captopril could affect the presynaptic site of the resistance vessels and cause a decrease in electrically-stimulated norepinephrine overflow from the adrenergic nerve endings. The marked reduction of the pressor responses and norepinephrine overflow to nerve stimulation by captopril in the SHR suggests that the renin-angiotensin system in the vascular beds in enhanced in this model of hypertension.

Animals↗
PubMed1987

Effects of nicardipine on blood pressure and platelet cytosolic free calcium concentration in SHR.

Intracellular free calcium concentration was measured by the fluorescent calcium indicator quin2 method in platelets of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and the effects of nicardipine on platelet cytosolic free calcium concentration were investigated. Cytosolic free calcium concentration was significantly increased in platelets of 4-, 11-, and 14-week-old SHR compared with age-matched WKY rats. Platelet cytosolic free calcium concentration in 14-week-old male SHR was significantly decreased 1 h after the administration of nicardipine (5 mg/kg p.o.), while that in WKY rats remained unchanged. These results suggest that transmembrane Ca2+ influx is genetically increased in SHR.

Administration, Oral↗
PubMed1987

Ca mobilization from the intracellular Ca store in spontaneously hypertensive rats.

To evaluate the size of the intracellular Ca store in spontaneously hypertensive rats (SHR), caffeine-induced contractions were investigated in mesenteric artery preparation. Twelve-week-old SHR and age-matched Wistar-Kyoto (WKY) rats were used. The isolated mesenteric artery was prepared by the method of McGregor. Caffeine (2 mg)- and norepinephrine (2 micrograms)-induced pressor responses were measured in both normal (Ca, 2 mM) and Ca-free solution (1 mM EGTA solution). In the presence of Ca, pressor responses to exogenous norepinephrine in SHR were higher than those in WKY rats. In Ca-free solution, pressor responses to norepinephrine were markedly reduced in SHR compared to WKY rats and caffeine-induced contractions in SHR were lower than those in WKY rats. These results suggest that pressor responses to norepinephrine in SHR may be more dependent on extracellular Ca than in WKY rats and the caffeine-sensitive intracellular Ca store might be less in SHR.

Animals↗
PubMed1987

[ECG-gated magnetic resonance imaging of the left ventricle: visualization of anatomical characteristics and quantification of wall thickness and ventricular volume in left ventricular hypertrophy].

Electrocardiography- and respiration-gated magnetic resonance imaging (MRI) was performed using a 0.15-Tesla resistive magnet system in 54 patients with left ventricular hypertrophy to define the site and extent of abnormal wall thickness and to estimate left ventricular function. Because the major cardiac axes are not orthogonal to the conventional transverse, sagittal or coronal planes, the long-axis and short-axis images of the left ventricle were obtained at the end-diastolic and end-systolic phases. The anatomic characteristics of concentric hypertrophy, asymmetric septal hypertrophy, and asymmetric apical hypertrophy were clearly demonstrated by MRI, even in patients with poor echocardiographic images. Quantitatively, left ventricular wall thicknesses obtained from MR images correlated well with those obtained from echocardiography (r = 0.95), and regression was y = 0.99x + 0.39, and so did the ratios of wall thickness of the interventricular septum to the left ventricular posterior wall (r = 0.91, y = 0.80x + 0.24). Left ventricular volumes calculated by the area-length method from MRI and those from left ventriculography also correlated well (r = 0.98, y = 1.13x + 24.5). In conclusion, using the gated long-axis and short-axis MR images of the left ventricle, the anatomical location and extent of hypertrophy and left ventricular volumes are noninvasively demonstrated.

Aged↗