Tohoku University · Medicine
Professor Masahiro Kohzuki's research lab specializes in cardiovascular and renal pharmacology, with a primary focus on the renin-angiotensin system and its role in hypertension, diabetic nephropathy, and end-organ damage. The lab investigates the renoprotective and antihypertensive effects of angiotensin receptor blockers and ACE inhibitors in animal models, particularly in diabetic and hypertensive rat models. A key research direction involves developing precise methods to measure active and inhibited forms of angiotensin-converting enzyme (ACE) in tissues, overcoming limitations of traditional enzymatic assays. The lab also explores the differential effects of RAS-modulating drugs on target organs such as the kidney and heart, contributing to a deeper understanding of drug mechanisms and tissue-specific responses.
Figures are computed from collected data and may differ slightly.
These results suggest that exercise does not worsen renal function and has renal-protective effects in this model of rats. Moreover, the antihypertensive therapy has additional renal-protective effects in this model of rats.
These results indicate that hypertension could accelerate diabetic renal impairment and that losartan has antihypertensive and renoprotective effects in this rat model. They also suggest that the antihypertensive and renoprotective effects of captopril treatment in this rat model are caused mainly by inhibition of angiotensin II production rather than stimulation of the kallikrein-kinin system or of vasodilator prostaglandins. The difference in potency between losartan treatment and captopril tr
Angiotensin converting enzyme (ACE) inhibitors lead to induction of ACE in animals and humans. This complicates the use of ACE enzymatic activity as an index of inhibition in plasma or tissues after chronic administration of ACE inhibitors. We have, therefore, developed a method for ACE measurement by in vitro autoradiography using an 125I-labelled inhibitor to quantitate total ACE and the concentration of free (not inhibited) ACE in tissues after prolonged administration of ACE inhibitors to ra
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