1986 Fiscal Year Final Research Report Summary
Membrane abnormalities in hypertension
| Project/Area Number |
60440049
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Division of Cardiology, Department of Medicine, Wakayama Medical College. |
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Principal Investigator |
MASUYAMA Yoshiaki Division of Cardiology, Wakayama Medical College, 医学部, 教授 (30089164)
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| Co-Investigator(Kenkyū-buntansha) |
KUCHII Masato Division of Cardiology, Wakayama Medical College, 循環器内科, 講師 (90073684)
NISHIO Ichiro Division of Cardiology, Wakayama Medical College, 循環器内科, 助教授 (40089165)
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| Project Period (FY) |
1985 – 1986
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| Keywords | Essential hypertension / Spontaneously hypertensive rats / Membrane abnormalities / Norepinephrine overflow / Vascular reactivity / Ca-Calmodulin system / Osmotic fragility / Erythrocyte membrane fluidity |
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| Research Abstract |
The purpose of this project was to elucidate the membrane abnormalities in hypertension. Firstly, we have examined alterations of synaptic membrane functions and sympathetic neurotransmission in blood vessels of hypertension. Isolated mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHR) and DOCA-salt hypertension in rats. The vasoconstrictor responses to electrical nerve stimulation or exogenous norepinephrine (NE) as well as endogenous NE overflow from the adrenergic nerve endings were significantly increased in young SHR and chronic DOCA-salt hypertension compared with their age-matched normotensive controls. The inhibitory modulations of NE overflow by presynaptic <alpha_2> -adrenoceptors, prostaglandin <E_2> ,dopamine, peptide hormones were attenuated in SHR than in controls. Whereas, the effects of Ca-antagonists, calmodulin-antagonists or <Na^+> , <K^+> -ATPase inhibitors on NE overflow were enhanced in these hypert antagonists or <Na^+> , <K^+> -ATPas
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e inhibitors on NE overflow were enhanced in these hypertensive models than in their controls.
Secondly, we have investigated physicochemical properties of cell membranes by use of erythrocytes obtained from patients with essential hypertension and SHR. The sodium content and Na-Li countertransport were increased in erythrocytes from essential hypertension compared with those in normotensive controls. Osmotic fragility of erythrocytes (determined by Coil Planet Centrifuge System) and erythrocyte membrane fluidity (determined by electron spin resonance method) were much affected by calcium. Further, these Ca-induced reductions of osmotic fragility and membrane fluidity were more prominent in essential hypertension and SHR compared with those in their normotensive controls.
These results suggest that alterations of synaptic membrane functions, attenuated responsiveness to vasodepressor hormones and abnormalities of physicochemical properties or Ca-sensitivity of the membranes could induce an exaggerated sympathetic nerve activity and vascular reactivity, which might contribute, at least partially, to the pathogenesis of hypertension. Less
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Research Products
(14 results)
