Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 145 records · Page 8Linked to original sources

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

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

The role of dopamine in the regulation of neurotransmitter release in spontaneously hypertensive rats.

The purpose of the present study was to analyze the influence of dopamine on norepinephrine release in resistance vessels in spontaneously hypertensive rats (SHR). Perfused mesenteric vasculature preparations from spontaneously hypertensive rats (7-10 weeks old) and age-matched normotensive Wistar Kyoto rats (WKY) were used to compare the effects of dopamine on both pressor responses and norepinephrine release. Both responses to electrical nerve stimulation were significantly greater in SHR than in WKY rats. Dopamine reduced these responses in a dose-dependent manner in WKY. However, this suppression of responses to electrical stimulation was attenuated in SHR. These results suggest that the enhanced adrenergic transmission in SHR may partly reflect impaired dopamine-mediated inhibition of nerve terminals, which would contribute to the pathogenesis of hypertension.

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

Comparative double-blind study of ketanserin versus propranolol in the treatment of essential hypertension.

To clarify the antihypertensive effect, safety and clinical usefulness of ketanserin, a comparative double-blind study was carried out in 277 patients with essential hypertension using propranolol as a control drug. Ketanserin 10 to 30 mg twice daily and propranolol 20 to 40 mg 3 times daily were administered for 12 weeks. The results showed no difference in antihypertensive effect and clinical usefulness between the drugs. In the ketanserine group, plasma concentration of total cholesterol was decreased significantly, and the reduction in heart rate was less than in the propranolol group. These findings suggest that ketanserin may satisfactorily control blood pressure.

Adult↗

PubMed1988

Contributions of the sympathetic nervous system, vasopressin and baroreceptor function in brain angiotensin II excess-induced hypertension in the dog.

To determine the principal effects of brain angiotensin(Ang) II on the sympathetic nervous system, vasopressin (AVP), and the high and low pressure baroreceptor systems, we observed the hemodynamic and neurohumoral characteristics induced by the acute(1-hr) and chronic(1-wk) infusion of Ang II into the brain ventricle in conscious dogs, and then evaluated the hemodynamic responses to sole-innervated carotid artery occlusion(COR) after Ang II infusion and again after vagotomy in anesthetized dogs. Both acute(50ng/kg/min) and chronic(15ng/kg/min) infusion of Ang II caused a significant rise in arterial pressure without changes in heart rate. Neither acute nor chronic Ang II treatment produced significant changes in plasma renin activity and norepinephrine in plasma and cerebrospinal fluid(CSF), while the plasma and CSF level of AVP was increased in the acute Ang II treatment, but not in the chronic Ang II treatment. The COR was blunted in the acute Ang II treatment compared with those obtained in the chronic Ang II or sham treatment. The blunted pressor response to carotid occlusion in the acute Ang II treatment was restored by cutting the remaining vagus nerve. These results suggest that baroreceptor reflexes are impaired by the acute excess of Ang II in the brain, and it might be mediated through increased vagal afferent activity, changes in the central integration of low and high pressure baroreceptors, and a combination of both.

Angiotensin II↗

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↗

PubMed1988