東北大学 · 의학
이 교수의 연구실은 신장 혈관 반응성과 내피 기능, 특히 엔도테리움에서 생성되는 일氧化화질소(EDRF/NO)가 신장 혈류동역학에 미치는 영향을 중심으로 연구를 진행하고 있습니다. 특히 아포트리큘러 동맥과 매크울라 덴사의 기능적 상호작용, 레닌-안지오텐신 시스템의 조절 메커니즘, 그리고 요독증에서 장내 미생물과 독소의 역할을 실험적으로 규명하고자 합니다. 최근에는 장내 미생물 조절제가 만성 신장질환의 진행에 미치는 영향을 연구하며, 임상적 응용 가능성을 탐색하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
