Tohoku University · 医学
伊藤沙大義教授の研究室は、腎臓の血流調節機構、特にアフェント動脈とマクラ・デンサの機能的相互作用に注目し、一酸化窒素（NO）やアンジオテンシンIIが腎小球血流に与える影響を、生体外マイクロプレッシャー法を用いて精密切に解析しています。特に、腎小管・血管インターフェースにおけるNOの局所的産生とその生理的役割、ならびに尿毒性物質と腸内細菌叢の関係についても、疾患モデルを用いてその病態解明を進めています。
Figures are computed from collected data and may differ slightly.
Although endothelium-derived relaxing factor (EDRF) has been studied extensively in large vessels, little is known about its role in the preglomerular afferent arteriole (Af-Art). We tested the hypothesis that EDRF, which is produced locally in the Af-Art, modulates arteriolar responses to angiotensin II (AII). A single rabbit Af-Art with its glomerulus intact was microperfused in vitro at 60 mmHg. When 0.1 microM AII was first applied, luminal diameter decreased by 49 +/- 7.0% (n = 9; P less th
Adding esaxerenone to existing renin-angiotensin system inhibitor therapy in patients with type 2 diabetes and microalbuminuria increased the likelihood of albuminuria returning to normal levels, and reduced progression of albuminuria to higher levels.
It has been reported that sensitivity to angiotensin II (Ang II) is higher in efferent (Ef) than afferent (Af) arterioles (Arts). We tested the hypothesis that this is due to arteriolar differences in the interaction between Ang II and endothelium-derived relaxing factor/nitric oxide (EDNO). Rabbit Af-Arts with glomerulus intact were microperfused in vitro at a constant pressure. Ef-Arts were perfused from the distal end of either the Af-Art (orthograde perfusion) or the Ef-Art (retrograde perfu
There is evidence that nitric oxide, an endothelium-derived relaxing factor, may be produced by the macula densa, as well as by blood vessels, within the kidney. To examine the role of nitric oxide in macula densa control of glomerular hemodynamics directly, we performed in vitro microperfusions of both rabbit afferent arterioles (with the glomerulus intact) and adherent tubular segments consisting of portions of the thick ascending limb, macula densa, and early distal tubule. While keeping affe
The accumulation of uremic toxins is involved in the progression of CKD. Various uremic toxins are derived from gut microbiota, and an imbalance of gut microbiota or dysbiosis is related to renal failure. However, the pathophysiologic mechanisms underlying the relationship between the gut microbiota and renal failure are still obscure. Using an adenine-induced renal failure mouse model, we evaluated the effects of the ClC-2 chloride channel activator lubiprostone (commonly used for the treatment
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