| Project/Area Number |
03454145
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Kagawa Medical School |
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Principal Investigator |
ABE Youichi Kagawa Medical School, Department of Pharmacology, Professor, 医学部, 教授 (10047227)
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| Co-Investigator(Kenkyū-buntansha) |
TAMAKI Toshiaki Kagawa Medical School, Department of Pharmacology, Assistant Professor, 医学部, 助教授 (80179879)
岩尾 洋 香川医科大学, 医学部, 助教授 (00137192)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1991: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | Renal hemodynamics / Renal blood flow / Afferent arteriole / Glomerulus / Angiotensin II / Vasopressin / Endothelium derived relaxing factor / Nitric oxide / L.ニトロ・アルギニン / 糸球体〓過量 / Lーニトロ-アルギニン / アンジオテンシンII / 自動性調節 |
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| Research Abstract |
Renal circulation is mainly regulated by two resistance vessels, the afferent arteriole and the efferent arteriole. Many experimental findings show that each arteriole has a different sensitivity to various kinds of physiological stimuli and vasoactive substances. Thus, for understanding the regulatory mechanisms of renal hemodynamics, it is very important to know whether or not sensitivity to vasoactive substances is different between the afferent and efferent arteriole. Angiotensin II(Ang II) and arginine vasopressin (AVP) are potent vasoconstrictors and they exert an important role to the regulation of renal hemodynamics. So, in the present study, we examined the effects of Ang II and AVP on the afferent arteriole in both in vitro and in vivo conditions, with special reference to endothelium derived relaxing factor(EDRF)-nitric oxide(NO).
1) in vitro experiment : The superficial afferent arterioles were microdissected from the kidney of New Zealand White rabbit. Each afferent arterio
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le was cannulate with a micropipette system, and the intraluminal pressure was set at 60 mmHg. We found that norepinephrine decreased the lumen diameter of the afferent arteriole in a dose-dependent manner, but Ang II even at high dose(10^<-6>M) did not affect the lumen diameter. However, after the pretreatment of L-NNA which is an inhibitor of NO synthase, Ang II constricted the afferent arteriole in a dose-dependent manner(10^<-12> - 10^<-10>M). AVP(10^<-6>M) slightly decreased the diameter, but the constrictor action of AVP was markedly enhanced by L-NNA.
2) in vivo experiment : Using pentobarbital -anesthetized dogs, we investigated whether or not vasopressin V2-receptor stimulation induced renal vasodilation and whether NO had a role in the process. Intrarenal infusion of AVP resulted in renal vasoconstriction. However, following pretreatment of a V1-antagonist, AVP caused a significant vasodilation. This vasodilation disappeared after the treatment of V2-antagonist. Even in the absence of the V2-antagonist, vasodilation was attenuated by intrarenal infusion of L-NNA.These findings clearly indicate that renal vasodilation is mediated by the V2 receptors. NO may participate in this renal vasodilation. Less
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