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Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 91 records · Page 5Linked to original sources
PubMed1991

Presynaptic regulation of neurotransmitter release in hypertension.

1. The present review discusses evidence in support of the concept that alterations in sympathetic neurotransmitter release might contribute to the pathogenesis of hypertension. 2. Studies suggest that changes in sympathetic nervous activity in both the central and peripheral nervous systems participate in blood pressure control. 3. In the periphery increased release of norepinephrine from vascular adrenergic neurons might lead to the enhanced vasoconstrictor responses and thus to an elevation in systemic blood pressure. 4. The amount of neurotransmitter release from sympathetic nerve endings can be regulated by autoregulatory systems by presynaptic receptors located on nerve terminals. 5. It has been proposed that alterations to sympathetic nervous activity of hypertension might be partially due to abnormalities in presynaptic modulation of neurotransmitter release in central and peripheral tissues. 6. This article summarizes the results of studies to evaluate presynaptic receptor functions and sympathetic neurotransmitter release in hypertension.

Animals↗
PubMed1991

Release of nerve growth factor from cultured aortic smooth-muscle cells.

Conditioned medium from cultured aortic smooth-muscle cells from rat aorta yielded neurite-extending effects on sensory and sympathetic ganglia of chick embryos. These effects were blocked by adding specific antiserum against 2.5S nerve growth factor (NGF), suggesting that NGF might be released from vascular smooth-muscle cells.

Animals↗
PubMed1991

Antihypertensive effects of oral calcium supplementation in spontaneously hypertensive rats.

This study was designed to clarify the mechanisms underlying the antihypertensive action of oral calcium supplementation in SHR. Four-week-old SHR and age-matched WKY were divided into calcium-supplemented and control groups. Calcium supplementation was carried out by giving 1.2% CaCl2 solution as drinking water ad libitum. Distilled water was given to the control group. After 3 weeks of treatment, plasma NE, pressor response to NE in isolated mesenteric artery, platelet cytosolic free calcium concentration and membrane fluidity of erythrocytes were evaluated. The elevation of blood pressure were retarded in calcium supplemented SHR. Calcium supplementation reduced the augmented pressor response to NE and the high level of cytosolic free calcium concentration in SHR. WKY showed no significant changes of these parameters by calcium supplementation. In conclusion, calcium supplementation reduces blood pressure through the reduction of sympathetic and vascular tone in SHR.

Administration, Oral↗
PubMed1991

Alterations in catecholamine release in the central nervous system of spontaneously hypertensive rats.

The aim of the present study was to investigate alterations in catecholamine release in the central nervous system of spontaneously hypertensive rats. Slices of hypothalamus, medulla oblongata and striatum were prepared from spontaneously hypertensive rats (SHR: 9-10 weeks old) and age-matched Wistar Kyoto rats (WKY). The slices were incubated with (3H)norepinephrine (NE) or (3H)dopamine (DA), superfused with Krebs-solution in vitro, and the release of the catecholamines was compared between the two strains. The basal release of hypothalamic (3H)NE did not differ between SHR and WKY slices. However, stimulation (1 Hz)-evoked (3H)NE release was significantly greater in SHR than in WKY (percent fractional release of total tissue NE: WKY 0.494 +/- 0.019%, n = 6, SHR 0.730 +/- 0.053%, n = 6, p less than 0.05). The stimulation-evoked (3H)NE release from the medulla oblongata did not differ significantly between SHR and WKY slices. Finally stimulation-evoked release of striatal (3H)DA was significantly depressed in SHR (percent fractional release of total tissue DA: WKY 2.048 +/- 0.24%, n = 6, SHR 1.460 +/- 0.068%, n = 6, p less than 0.05). These results indicate that the release of hypothalamic NE and striatal DA are altered in SHR. It is suggested that enhanced hypothalamic noradrenergic activity and reduced striatal dopaminergic activity can increase sympathetic outflow to the periphery, which may play a role in the pathogenesis of this form of hypertension.

Animals↗
PubMed1991

Altered renin release from isolated superfused rat glomeruli in DOCA-salt hypertensive rats.

The present study was designed to clarify the role of calcium in suppressed renin release in DOCA-salt hypertension. Rat glomeruli were isolated by the modified Beierwaltes' sieving method. The glomeruli were superfused with Krebs-Ringer solution. Basal levels of renin release were lower in the DOCA-salt hypertensive rats (1.16 +/- 0.27 ng/ATI/hr/hr/10(4) glomeruli, mean +/- SEM, n = 8) than in the control rats (1.92 +/- 0.18, p less than 0.01, n = 8). Perfusion with a calcium free solution containing EGTA and A23187 stimulated renin release in the DOCA-salt hypertensive and control rats. The maximum levels of renin release during the perfusion in DOCA-salt hypertensive rats (1.79 +/- 0.17, n = 8) were lower than those in control rats (10.60 +/- 1.85, p less than 0.01, n = 8). These results suggest that high levels of intracellular calcium might not contribute to the suppression of renin release in DOCA-salt hypertension.

Animals↗
PubMed1991

[Effects of calcium antagonist, angiotensin-converting enzyme inhibitors and beta-blocker on hemodynamic and sympathetic nerve responses to exercise in essential hypertension].

To investigate the effects of antihypertensive drugs on hemodynamic and sympathetic nerve responses to exercise, graded ergometer exercise tests were performed before and after two-week administration of nifedipine, captopril and metoprolol in 18 patients with essential hypertension. The arterial pressure, heart rates (HR), and left ventricular functions as obtained by echocardiography, and the plasma norepinephrine (PNE) levels, were evaluated at rest and during submaximal exercise before and after two-week treatment with nifedipine (40 mg/day, 5 cases), captopril (37.5-75 mg/day, 6 cases) and metoprolol (60 mg/day, 7 cases). These 3 drugs significantly reduced systolic (SBP) and diastolic (DBP) blood pressures but caused no significant changes in resting PNE levels. Nifedipine produced no significant changes in HR and cardiac output (CO) at rest, but augmented the increase in HR (delta HR) and SBP (delta SBP) during submaximal exercise. The increase in PNE (delta PNE) was also augmented by nifedipine. Captopril reduced left ventricular end-diastolic volume and CO without changes in HR and fractional shortening (FS) at rest; whereas, it did not affect delta HR, delta CO, delta SBP or delta PNE during exercise. Metoprolol reduced HR and CO at rest, and also resulted in a decrease in delta FS and delta CO during submaximal exercise. delta SBP was unchanged and delta PNE was increased by treatment with metoprolol. These results indicate that, in hypertensive subjects, the effects on the hemodynamic and sympathetic nerve responses to exercise are different among these 3 antihypertensive drugs despite their identical effects on blood pressure.

Adrenergic beta-Antagonists↗
PubMed1991

[Observation of bleeding sites by fiberoptic bronchoscopy in a case of vasculo-Behçet's disease with pulmonary involvement].

A 45-year-old man complained of fever and bloody sputum. Chest X-ray films showed a round opacity in the left hilum. He developed massive hemoptysis (500 ml) and emergency embolization of the bronchial artery was performed. Pulmonary artery aneurysm and thrombosis were detected angiographically, and fiberoptic bronchoscopy revealed a reddish irregular eminence of the left main bronchus and lingulate++ ++ bronchus. These sites could have been the bleeding sites. Because of recurrent hemoptysis, left pneumonectomy was performed 26 days after the massive hemoptysis. Pathological findings showed panarteritis, luminal thromboembolism of the pulmonary artery and markedly dilated vessels of the bronchial wall. He developed genital ulceration after the operation and these findings suggested incomplete vasculo-Behçet's disease with rare pulmonary involvement. The disease is now well-controlled by corticosteroid therapy 27 months after the operation.

Aneurysm↗
PubMed1991

[A case report of Creutzfeldt-Jakob disease associated with myocarditis].

We have encountered a case of Creutzfeldt-Jakob disease associated with myocarditis. A 77 year-old woman was admitted to a hospital with complaints of rapidly progressive visual disturbance, myoclonus and dementia. Electroencephalogram revealed a periodic synchronous discharge and Creutzfeldt-Jakob disease was suspected. Then she moved to our hospital, because acute myocarditis was combined with ST-T changes on electrocardiogram, and generalized hypokinetic motion of the left ventricle on echocardiogram. The abnormal findings in electrocardiography and echocardiography were transient. Blood levels of enzymes derived from the myocardium were slightly elevated. We could not find a distinct increase in the titer of neutralizing antibody to various viruses. In this case, the cause of myocarditis may have been associated with the infectious agent of Creutzfeldt-Jakob disease. This report might be the first one with a case of Creutzfeldt-Jakob disease complicated with myocarditis.

Aged↗
PubMed1990

Effects of calcitonin gene-related peptide on [3H]norepinephrine release in medulla oblongata of spontaneously hypertensive rats.

We now describe the effects of calcitonin gene-related peptide (CGRP) on [3H]norepinephrine (NE) release in medulla oblongata of spontaneously hypertensive rats (SHR). CGRP inhibited stimulation-evoked [3H]NE release in a dose-dependent manner in Sprague-Dawley rats, although the basal release of [3H]NE was not affected by the peptide. In SHR, the inhibitory effect of CGRP on stimulation-evoked [3H]NE release was significantly attenuated compared with Wistar Kyoto rats. These results suggest that CGRP might be involved in the regulation of central sympathetic nervous activity in hypertension.

Animals↗
PubMed1990

Effects of neuropeptide Y on norepinephrine release in hypothalamic slices of spontaneously hypertensive rats.

We describe the effects of neuropeptide Y (NPY) on [3H]norepinephrine (NE) release from hypothalamic slices of spontaneously hypertensive rats (SHR). The electrical stimulation (1 Hz)-evoked [3H]NE release was significantly greater in hypothalamic slices of SHR than in those of Wistar Kyoto rats (WKY). NPY inhibited the stimulation-evoked [3H]NE release in a dose-dependent manner. The inhibitory effect of NPY was significantly attenuated in SHR compared with WKY. The results may indicate that the less inhibitory effect of NPY on NE release induces increased sympathetic nerve activity in the hypothalamus of SHR.

Animals↗
PubMed1990

Enhanced DNA synthesis of cultured vascular smooth muscle cells from spontaneously hypertensive rats. Difference of response to growth factor, intracellular free calcium concentration and DNA synthesizing cell cycle.

It is widely reported that cultured vascular smooth muscle cells (CVSMCs) from spontaneously hypertensive rats (SHR) show enhanced proliferation compared with cells from Wistar-Kyoto rats (WKY). The present studies were designed to find out whether this exaggerated proliferation in SHR is determined genetically and, if so, to evaluate the mechanism on the cell cycle. (1) Incorporation of [3H]thymidine into DNA was enhanced in CVSMCs from 3- and 12-week-old SHR compared with WKY but not in CVSMCs from DOCA-salt hypertensive rats compared with the cells from sham-operated rats. (2) DNA synthesis in SHR cells was enhanced further by addition of insulin (which is considered to be a progression factor) but not by arginine-vasopressin (AVP; considered to be a competence factor) or by angiotensin II (AII). On the other hand, insulin, AVP and AII significantly augmented DNA synthesis in WKY cells. (3) Intracellular free calcium concentration was slightly, but significantly, higher in SHR cells. (4) An increase in the population of DNA-synthesizing S-phase cells and decrease in (G2 + M)-phase cells in SHR were observed by flowcytometry. These data suggest (1) that enhanced DNA synthesis in CVSMCs from SHR is determined genetically, (2) that enhanced DNA synthesis in CVSMCs from SHR is largely dependent on an increased proportion of S-phase cells and (3) that this increase in S-phase cells in CVSMCs from SHR could be due to enhanced competence gene expression in SHR cells. (4) The increased intracellular free calcium concentration is compatible with an activation of the inositol-trisphosphate pathway.

Angiotensin II↗
PubMed1990

Effect of centrifugal force and catecholamines on glycosaminoglycans synthesis of vascular smooth muscle cells in culture.

To evaluate the effect of hypertension on glycosaminoglycan (GAG) synthesis, cultured vascular smooth muscle cells (CVSMCs) from the aorta of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were exposed to centrifugal forces and catecholamines. GAG synthesis of CVSMCs was measured by the incorporation of [3H]glucosamine into GAGs which were secreted into the culture medium for 24 h. Basal level of GAG synthesis was much higher in SHR than in WKY, when expressed in terms of DNA contents. When exposed to centrifugal force, CVSMCs from rats of both strains synthesized more GAGs. GAG synthesis was enhanced by both noradrenaline (NA) and adrenaline (Ad) in WKY. The enhanced GAG synthesis in WKY by NA or Ad was prevented by pretreatment with propranolol, but not prazosin. In SHR, NA and Ad did not enhance GAG synthesis at this concentration of catecholamines. However, the effects of propranolol or prazosin on GAG synthesis in SHR, when incubated with either NA or Ad, were compatible with the phenomena observed in WKY. Adding dibutyryl cyclic AMP to the culture medium enhanced GAG synthesis in rats of both strains. These data suggest that not only the mechanical stress of high intra-arterial pressure but also beta receptor stimulation, via increasing cyclic AMP, enhance GAG synthesis of vascular smooth muscle cells in hypertension.

Animals↗
PubMed1990

Enhanced endogenous epinephrine release from the vascular adrenergic neurons in spontaneously hypertensive rats.

This study was performed to investigate the role of endogenous epinephrine in the regulation of vascular tone in hypertension. The release of endogenous epinephrine and norepinephrine from the vascular adrenergic neurons by periarterial nerve stimulation was examined in spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). The isolated mesenteric vasculatures were prepared, and the epinephrine and norepinephrine release during electrical nerve stimulation was determined as the increase in epinephrine and norepinephrine contents in the vascular perfusate. Epinephrine and norepinephrine were measured by high performance liquid chromatography with an electrochemical detector. Vasoconstrictor responses and norepinephrine overflow during electrical nerve stimulation were significantly greater in SHR than in WKY. The amount of stimulation-evoked epinephrine overflow into the perfusate was also increased in SHR compared to that in WKY, especially at low frequency stimulation. These results suggest that epinephrine could be released from the vascular adrenergic neurons as a cotransmitter of norepinephrine and contribute to increased vascular tone in hypertension.

Animals↗
PubMed1990

Neuropeptide Y and galanin enhance the inhibitory effects of clonidine on norepinephrine release from medulla oblongata of rats.

The medulla oblongata is thought to play an important role in the central regulation of blood pressure. Neuropeptide Y (NPY) and galanin (Gal) coexist with norepinephrine (NE) and may have a functional interaction in this region. The aim of the present study was to investigate whether NPY and Gal could modulate the presynaptic neuronal mechanisms, especially the alpha-adrenoceptor function, inhibiting NE release in medulla oblongata. In slices of rat medulla oblongata, clonidine, an alpha-adrenoceptor agonist, inhibited the NE release elicited by electrical stimulation in a concentration-dependent manner. A combination of clonidine and low concentration of NPY (1 X 10(-9) mol/L) resulted in an increase in the inhibitory action of clonidine on stimulation-evoked NE release. The inhibitory action of clonidine was also potentiated by Gal (1 X 10(-8) mol/L). These results indicate the existence of the presynaptic NPY- and Gal-receptors on noradrenergic nerve terminals, which may enhance the presynaptic alpha-adrenoceptor function to inhibit NE release. This suggests a possible involvement of NPY and Gal in the regulation of sympathetic nerve activity in medulla oblongata.

Animals↗
PubMed1990

The role of protein kinase C and calcium in the regulation of norepinephrine release from the vascular adrenergic neurons in hypertension.

This study was designed to investigate the role of protein kinase C and calcium in vascular adrenergic transmission in hypertension. In perfused mesenteric vasculatures of spontaneously hypertensive rats (SHR, 7 to 10 weeks old) and age-matched Wistar-Kyoto rats (WKY), we have examined the effects of the protein kinase C inhibitor H-7 on endogenous norepinephrine release and vascular responsiveness during nerve stimulation. Endogenous norepinephrine release and pressor responses during periarterial nerve stimulation were significantly greater in SHR than in WKY. The protein kinase C inhibitor H-7 inhibited the stimulation-induced norepinephrine release and pressor responses in a dose-dependent manner. The magnitude of these suppressive responses were more pronounced in SHR than in WKY. Calcium removal from extracellular fluid also reduced the norepinephrine release more strongly in SHR than in WKY. These results demonstrate that the regulation of norepinephrine release might be more dependent on protein kinase C and calcium in the blood vessels of SHR, which could contribute, at least partially, to the pathogenesis of this form of hypertension.

Animals↗
PubMed1990

Deficient activity of nucleotide binding regulatory protein coupled with PGE2 receptor in renal medulla of spontaneously hypertensive rats.

Prostaglandin (PG) E2 receptor-adenylate cyclase system was studied in the kidney of 12-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to evaluate the role of this system in hypertension. PGE2 receptors were determined by a radioligand binding method using [3H]-PGE2. Adenylate cyclase responses to PGE2, sodium fluoride (NaF) and forskolin were also measured. The concentration of PGE2 receptor was increased in SHR compared with WKY. PGE2- and NaF-stimulated adenylate cyclase activities were significantly lower in SHR than WKY. There was no significant difference in forskolin-stimulated adenylate cyclase activity between SHR and WKY. NaF activates the nucleotide binding regulatory protein (G-protein) and forskolin directly activates the catalytic unit. These results indicate that the activity of G-protein coupled with renal PGE2 receptors is deficient in SHR. This defect may contribute to the elevation of blood pressure, through sodium retention.

Adenylyl Cyclases↗