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• W3126232112 abstract "By use of intravital multiphoton microscopy, Ziegler et al. address a role of renal mesangial cells for glomerular capillary dynamics (see the current issue of Acta Physiologica).1 High and constant glomerular filtration rate (GFR) is a main priority in the organism to ensure rapid adaptation to salt and water intake and to warrant low concentrations in plasma of soluble waste products. GFR is tightly autoregulated by glomerular afferent and efferent arteriolar resistances. A question that has puzzled kidney physiologists for decades is whether the mesangial cells have regulatory or perhaps modulatory function on GFR. Mesangial cells are contractile and supportive cells in contact with glomerular arterioles and intraglomerular capillaries in the glomerular tuft. It has been experimentally challenging to analyse a role for mesangial cells in the control of filtration surface area, hydraulic conductivity and arteriolar/capillary resistance. Ziegler et al use anti-Thy1.1 antibody to selectively delete mesangial cells in adult rats and employ a strain of rats with superficial glomeruli for direct intravital imaging. By using angiotensin II (ANGII) and noradrenaline in combination with labelled albumin this approach revealed dynamic changes in capillary diameters, flow, filtration and overall capillary movements confirming a contribution of mesangial cells. Zimmerman et al. in 1933, were the first to describe the glomerular mesangium. Mesangial cells are specialized contractile cells associated with the kidney glomeruli where they form a continuous network bridging the glomerular tuft where afferent and efferent arterioles pass into the renal corpuscle. They are in contact with glomerular capillaries in a small area called the juxtamesangial portion. They produce a rich extracellular matrix, communicate with other cell types, provide mechanical support, proliferate, take up macromolecules from the extracellular space and are associated with glomerular pathologies. In diabetic nephropathy mesangial cells hypertrophy and the mesangial matrix is expanded. Mesangial cells contain bundles of contractile filaments2 and in some aspects resemble smooth muscle cells: They have negative membrane potentials; they depolarize by exposure to ANGII through calcium-activated chloride channels3 to increase intracellular calcium concentration,4 which results in contraction as judged by morphology changes in single cells in culture. These properties led to the proposal of a functional role of the mesangium. In 1976, Blantz et al., performed experiments with micropuncture technique in the same rat strain that authors employed in the present issue of Acta.5 They could show that net ultrafiltration pressure increases after ANGII and essentially neutralizes the effect of decreased renal plasma flow on single nephron GFR.5 The ultrafiltration coefficient Kf (the product of effective filtration surface area and hydraulic conductivity) was reduced in that study. The authors put forward a role for mesangial cells for these changes in Kf through reduced glomerular capillary filtration surface area. The view was extended by Dworkin et al. who suggested in 19836 that despite a fall in renal plasma flow with neurohumoral activation by, for example, ANGII and fall in Kf, GFR could be partially maintained through increased ultrafiltration pressure gradient. For obvious reasons, this concept on a role for mesangial cells is difficult to resolve by micropuncture techniques alone. Thus, attempts to address the issue were done in fixed tissue from the same strain of rats. In volume-contracted rats, the glomerular tuft area was reduced significantly.7 Ziegler et al. set out to gain more information by application of high-resolution fluorescence microscopy, thereby allowing real-time visualization of in vivo events. They focused on targeting mesangial cells by an immune-mediated destruction to elucidate changes in baseline glomerular parameters. Then the authors challenged the model by in vivo exposure to ANGII.1 They observed that mesangial cell depletion lowers baseline GFR and capillary linear flow velocity; ANGII infusion decreased capillary flow velocity similarly in control rats but had no further effect after mesangial cell depletion. Mesangial cell lysis caused a significant dilatation of capillaries and with the decreased linear flow velocity the calculated flow rate remained constant. This finding is striking considering the marked decrease in GFR, it indicates either a decreased surface area or lower ultrafiltration pressure. One notable finding was a rotational-contractile movement of the entire set of glomerular capillaries in the direction of the glomerular stalk in response to ANGII, which was absent after mesangial cell depletion.1 This could be a first direct observation in vivo of integrated mesangial contractile action since it was independent of afferent arteriolar diameter change and also not dependent on the parallel blood pressure increase. These are important controls because mesangial cells have direct contact to afferent arterioles. In further support, the authors documented the response as associated with single mesangial cell contraction.1 The experiments do not resolve the reason behind the significant lowering of single-nephron GFR after mesangial cell depletion. The Munich-Frömter rat strain was used which is prone to inherited nephron deficit with mild hypertension and progressive albuminuria and male preponderance8 However, female rats were used with no hypertension compared to controls. Perhaps confounding immunological injury was involved in the lower GFR after mesangial cell lysis. Antibody-driven mesangial destruction was employed, which depends on complement system activation through the classical pathway with ultimate cell lysis. The authors did document that the primary antibody is selective in targeting mesangial cells and not podocytes. However, the complement system response may induce local amplification through release of the anaphylatoxins C3a and C5a, which have renal receptors that may amplify local inflammation. The very marked local dilatation of glomerular capillaries after mesangial cell lysis may be influenced by such a response. With these cautions in mind, Ziegler et al provide important new in vivo information at the very edge of what is technically possible on the exclusive and scarce mesangial cells and their involvement in glomerular capillary dynamics and filtration. The author declares no conflict of interest." @default.
• W3126232112 created "2021-02-15" @default.
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• W3126232112 date "2021-02-12" @default.
• W3126232112 modified "2023-09-23" @default.
• W3126232112 title "Live imaging of kidneys in vivo reveals impact of mesangial cells on glomerular capillaries and potential role in glomerular filtration" @default.
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• W3126232112 doi "https://doi.org/10.1111/apha.13618" @default.
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