Intraglomerular microcirculation: Measurements of single glomerular loop flow in rats

Steinhausen, M.; Zimmerhackl, B.; Thederan, H.; Dussel, R.; Parekh, N.; Eβlinger, Hans-Ulrich; Hagens, Gunther von; Komitowski, D.; Dallenbach, Friederike

doi:10.1038/ki.1981.125

Cited by 35 publications

(7 citation statements)

References 25 publications

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“…1,[31][32][33][34][35] Previous publications also reported on different invasive in situ preparation techniques to assess vascular parameters such as renal blood flow, flow velocity, and vessel diameter in experimental kidney injury models in rats. [36][37][38][39][40][41][42][43][44][45][46] However, highly detailed longitudinal analyses on vessel functionality in experimental mouse models of chronic kidney diseases have not been performed to date. To bridge this gap, we refined a recently described contrast-enhanced mCT-based imaging protocol enabling the noninvasive visualization and quantification of microvascular changes in tumors and in liver fibrosis 18,19 for monitoring vessel functionality in experimental models of chronic kidney injury in mice.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Ehling¹,

Bábíčková

Gremse

et al. 2016

Journal of the American Society of Nephrology

124

131

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Progressive kidney diseases and renal fibrosis are associated with endothelial injury and capillary rarefaction. However, our understanding of these processes has been hampered by the lack of tools enabling the quantitative and noninvasive monitoring of vessel functionality. Here, we used micro-computed tomography (mCT) for anatomical and functional imaging of vascular alterations in three murine models with distinct mechanisms of progressive kidney injury: ischemia-reperfusion (I/R, days 1-56), unilateral ureteral obstruction (UUO, days 1-10), and Alport mice (6-8 weeks old). Contrast-enhanced in vivo mCT enabled robust, noninvasive, and longitudinal monitoring of vessel functionality and revealed a progressive decline of the renal relative blood volume in all models. This reduction ranged from 220% in early disease stages to 261% in late disease stages and preceded fibrosis. Upon Microfil perfusion, high-resolution ex vivo mCT allowed quantitative analyses of three-dimensional vascular networks in all three models. These analyses revealed significant and previously unrecognized alterations of preglomerular arteries: a reduction in vessel diameter, a prominent reduction in vessel branching, and increased vessel tortuosity. In summary, using mCT methodology, we revealed insights into macro-to-microvascular alterations in progressive renal disease and provide a platform that may serve as the basis to evaluate vascular therapeutics in renal disease.

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Section: Discussionmentioning

confidence: 99%

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Ehling¹,

Bábíčková

Gremse

et al. 2016

Journal of the American Society of Nephrology

124

131

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“…1, 2, 3. Third, the model can be applied to different rat strains, including the Munich Wistar rats in which many glomeruli are located directly under the vicinal surface of the kidney cortex, 10,11) and genetically modified Sprague Dawley rats, for instance, transgenic rats carrying the enhanced green fluorescent protein (EGFP) transgene. 12,13) …”

Section: Establishment Of An Experimental Model Of Progressive Glomermentioning

confidence: 99%

Exploring the mechanisms of renoprotection against progressive glomerulosclerosis

Oite

2011

Proceedings of the Japan Academy. Ser. B: Physical and Biologic

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In this review, I introduce the strategy developed by our laboratory to explore the mechanisms of renoprotection against progressive glomerulosclerosis leading to renal death. First, I describe the experimental rat model in which disturbances of vascular regeneration and glomerular hemodynamics lead to irreversible glomerulosclerosis. Second, I discuss the possible mechanisms determining the progression of glomerulosclerosis and introduce a new imaging system based on intravital confocal laser scanning microscopy. Third, I provide an in-depth review of the regulatory glomerular hemodynamics at the cellular and molecular levels while focusing on the pivotal role of Ca2+-dependent gap junctional intercellular communication in coordinating the behavior of mesangial cells. Last, I show that local delivery of renoprotective agents, in combination with diagnostic imaging of the renal microvasculature, allows the evaluation of the therapeutic effects of angiotensin II receptor and cyclooxygenase activity local blockade on the progression of glomerulosclerosis, which would otherwise lead to renal death.

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“…To visualize the glomerular microvasculature, we used the technique of hydronephrosis (13,25,48,49). Given the possibility that the process of hydronephrosis may have impacted upon glomerular function, we examined various parameters to assess the inflammatory response in glomeruli of hydronephrotic kidneys.…”

Section: Figure 10mentioning

confidence: 99%

Leukocyte Recruitment to the Inflamed Glomerulus: A Critical Role for Platelet-Derived P-Selectin in the Absence of Rolling

Kuligowski

Kitching

Hickey

2006

The Journal of Immunology

122

153

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The renal glomerulus is one of the few sites within the microvasculature in which leukocyte recruitment occurs in capillaries. However, due to the difficulty of directly visualizing the glomerulus, the mechanisms of leukocyte recruitment to glomerular capillaries are poorly understood. To overcome this, we rendered murine kidneys hydronephrotic to allow the visualization of the functional glomerular microvasculature during an inflammatory response. These experiments demonstrated that following infusion of anti-glomerular basement membrane (GBM) Ab, leukocytes became adherent in glomerular capillaries via a process of immediate arrest, without undergoing prior detectable rolling. However, despite the absence of rolling, this recruitment involved nonredundant roles for the P-selectin/P-selectin glycoprotein ligand-1 and β2 integrin/ICAM-1 pathways, suggesting that a novel form of the multistep leukocyte adhesion cascade occurs in these vessels. Anti-GBM Ab also increased glomerular P-selectin expression and induced a P-selectin-independent increase in platelet accumulation. Moreover, platelet depletion prevented both the increase in glomerular P-selectin, and the leukocyte recruitment induced by anti-GBM Ab. Furthermore, depletion of neutrophils and platelets also prevented the increase in urinary protein excretion induced by anti-GBM Ab, indicating that their accumulation in glomeruli contributed to the development of renal injury. Finally, infusion of wild-type platelets into P-selectin-deficient mice restored the ability of glomeruli in these mice to support leukocyte adhesion. Together, these data indicate that anti-GBM Ab-induced leukocyte adhesion in glomeruli occurs via a novel pathway involving a nonrolling interaction mediated by platelet-derived P-selectin.

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Intraglomerular microcirculation: Measurements of single glomerular loop flow in rats

Cited by 35 publications

References 25 publications

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Exploring the mechanisms of renoprotection against progressive glomerulosclerosis

Leukocyte Recruitment to the Inflamed Glomerulus: A Critical Role for Platelet-Derived P-Selectin in the Absence of Rolling

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