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Mizuo Miyazaki

Researcher at Osaka Medical College

Publications -  233
Citations -  8455

Mizuo Miyazaki is an academic researcher from Osaka Medical College. The author has contributed to research in topics: Angiotensin II & Chymase. The author has an hindex of 49, co-authored 233 publications receiving 8200 citations. Previous affiliations of Mizuo Miyazaki include Osaka City University.

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Angiotensin II type 2 receptor overexpression activates the vascular kinin system and causes vasodilation.

TL;DR: The results suggest that AT2 in aortic VSM cells stimulates the production of bradykinin, which stimulates the NO/cGMP system in a paracrine manner to promote vasodilation, which is predicted to have a beneficial clinical effect in controlling blood pressure.
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Nox1 Is Involved in Angiotensin II–Mediated Hypertension A Study in Nox1-Deficient Mice

TL;DR: A pivotal role for ROSs derived from Nox1/NADPH oxidase was suggested in the pressor response to Ang II by reducing the bioavailability of nitric oxide.
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Bone marrow monocyte lineage cells adhere on injured endothelium in a monocyte chemoattractant protein-1-dependent manner and accelerate reendothelialization as endothelial progenitor cells

TL;DR: BM-MLCs can function as EC progenitors that are more potent than CD34+ cells and acquire the ability to adhere on injured endothelium in a MCP-1–dependent manner, leading to reendothelialization associated with inhibition of intimal hyperplasia.
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Vascular renin-angiotensin system in two-kidney, one clip hypertensive rats.

TL;DR: The results suggest that the vascular renin-angiotensin system plays an important role in the maintenance of two-kidney, one clip hypertension.
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Evidence for a putatively new angiotensin II-generating enzyme in the vascular wall.

TL;DR: Results strongly suggest that besides the ANG I converting enzyme, another enzyme which generates ANG II is present in vascular tissues and lungs, and may play an important role in the local generation of ANG II, which possibly regulates the regional vascular tone.