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Makoto Mizuno

Researcher at Daiichi Sankyo

Publications -  26
Citations -  727

Makoto Mizuno is an academic researcher from Daiichi Sankyo. The author has contributed to research in topics: Prasugrel & Angiotensin II receptor antagonist. The author has an hindex of 10, co-authored 26 publications receiving 661 citations.

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Anti-Hypertensive Agents Inhibit In Vivo the Formation of Advanced Glycation End Products and Improve Renal Damage in a Type 2 Diabetic Nephropathy Rat Model

TL;DR: It is concluded that AGE inhibition should be included in the therapeutic strategy of DN after a strain of spontaneously hypertensive/NIH-corpulent rats was used as a model of type II DN to unravel the renoprotective effects of anti-hypertensive drugs.
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Nonpeptide Angiotensin II Receptor Antagonists: Synthesis, Biological Activities, and Structure−Activity Relationships of Imidazole-5-carboxylic Acids Bearing Alkyl, Alkenyl, and Hydroxyalkyl Substituents at the 4-Position and Their Related Compounds

TL;DR: A series of imidazole-5-carboxylic acids bearing alkyl, alkenyl, and hydroxyalkyl substituents at the 4-position and their related compounds were prepared and evaluated for their antagonistic activities to the angiotensin II (AII) receptor.
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Pharmacology of CS-866, a novel nonpeptide angiotensin II receptor antagonist

TL;DR: It is demonstrated that RNH-6270 is a potent and AT1-selective angiotensin receptor antagonist and that, after oral administration, CS-866 has a long-lasting ang Elliotensin II inhibitory action which is not affected by drug metabolizing enzymes in the liver.
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Pharmacological profile of CS-3150, a novel, highly potent and selective non-steroidal mineralocorticoid receptor antagonist

TL;DR: It is indicated that CS-3150 is a selective and highly potent mineralocorticoid receptor antagonist with long-lasting oral activity and could be useful for the treatment of hypertension, cardiovascular and renal disorders.
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Activation of renal angiotensin type 1 receptor contributes to the pathogenesis of progressive renal injury in a rat model of chronic cardiorenal syndrome

TL;DR: The pathogenetic role of renal interstitial AT1R signaling in a model of type 2 cardiorenal syndrome is demonstrated, providing evidence that AT 1R blockade can be a useful therapeutic option for this syndrome.