Renal cortical interstitium and fluid absorption by peritubular capillaries

Aukland, Knut; Bogusky, Ronald T.; Renkin, Eugene M.

doi:10.1152/ajprenal.1994.266.2.f175

Cited by 21 publications

(20 citation statements)

References 34 publications

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“…Lymphatic vessels contribute to the drainage of extravasated proteins, excess fluid and macromolecules from interstitial tissue and return them to the blood circulation via the lymph, playing a crucial role in tissue fluid balance and homeostasis [14], [15]. They are also essential for immune defense by carrying antigens and antigen-presenting cells from the interstitium to the lymph nodes, a critical step for the development of an immune response [16].…”

Section: Introductionmentioning

confidence: 99%

Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis

et al. 2012

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Proteinuria is an important cause of progressive tubulo-interstitial damage. Whether proteinuria could trigger a renal lymphangiogenic response has not been established. Moreover, the temporal relationship between development of fibrosis, inflammation and lymphangiogenesis in chronic progressive kidney disease is not clear yet. Therefore, we evaluated the time course of lymph vessel (LV) formation in relation to proteinuria and interstitial damage in a rat model of chronic unilateral adriamycin nephrosis. Proteinuria and kidneys were evaluated up to 30 weeks after induction of nephrosis. LVs were identified by podoplanin/VEGFR3 double staining. After 6 weeks proteinuria was well-established, without influx of interstitial macrophages and myofibroblasts, collagen deposition, osteopontin expression (tubular activation) or LV formation. At 12 weeks, a ∼3-fold increase in cortical LV density was found (p<0.001), gradually increasing over time. This corresponded with a significant increase in tubular osteopontin expression (p<0.01) and interstitial myofibroblast numbers (p<0.05), whereas collagen deposition and macrophage numbers were not yet increased. VEGF-C was mostly expressed by tubular cells rather than interstitial cells. Cultured tubular cells stimulated with FCS showed a dose-dependent increase in mRNA and protein expression of VEGF-C which was not observed by human albumin stimulation. We conclude that chronic proteinuria provoked lymphangiogenesis in temporal conjunction with tubular osteopontin expression and influx of myofibroblasts, that preceded interstitial fibrosis.

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Section: Introductionmentioning

confidence: 99%

Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis

et al. 2012

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“…In the gastrointestinal tract and the cortex of the kidney, where the epithelial secretion of large volumes of protein-free fluid dilute the interstitial fluid, steady reabsorption into the blood vessels can occur as long as lymphatics are available to drain excess fluid and protein. Aukland, Bogusky & Renkin (1994) have recently developed this hypothesis for uptake of fluid by renal cortical capillaries under normal conditions. In the renal medulla, however, where significant amounts of water are reabsorbed during urine concentration, the situation is more complex.…”

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confidence: 99%

Subatmospheric closing pressures in individual microvessels of rats and frogs.

MacPhee

Michel

1995

The Journal of Physiology

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1. We have investigated the hypothesis that ascending vasa recta (AVR) in the rat renal medulla are able to remain open when the external pressure is greater than the internal. 2. Individual vasa recta were cannulated in anaesthetized rats with Evans Blue albumin solution and then occluded downstream prior to the first branchpoint. When the intraluminal pressure was lowered, the lumina collapsed at a mean pressure of approximately -4 0 cmH2O for both AVR and descending vasa recta. 3. The studies were extended to include microvessels from rat spinotrapezius muscle and mesentery and frog mesentery; mean closing pressures were -32, -4-2 and -5-3 cmH2O, respectively.

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“…It is now well recognized that a highly regulated glomerular microcirculation (glomerular hemodynamics) is essential for this precise control of the GFR. 1,2 Although the juxtaglomerular apparatus (JGA) has long been suggested to play a central role in the control of glomerular hemodynamics, by adjusting the balance of vascular resistance in preglomerular afferent (Af-) and postglomerular efferent arterioles (Ef-Arts), 3 attempts to obtain direct evidence have been hindered by its anatomical complexity. Recently, microdissection and perfusion methods have been successfully employed for the direct assessment of JGA function, 4,5 contributing to our understanding of the mechanisms that control glomerular hemodynamics.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms that control glomerular hemodynamics

Arima

Kohagura

Abe

et al. 2001

Clinical and Experimental Nephrology

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The balance of the vascular tone between afferent (AfArts) and efferent arterioles (Ef-Arts) is a crucial determinant of glomerular hemodynamics. In order to directly study the mechanisms that regulate their vascular tone, we have developed several in-vitro microperfusion preparations of these arterioles, which allow us to observe the arteriolar diameter in the absence of systemic hemodynamic and hormonal influences. In the Af-Art, but not Ef-Art, we have demonstrated the presence of two intrinsic mechanisms, myogenic response and macula densa-mediated tubuloglomerular feedback, both of which play an important role in the control of vascular tone. We also found that both of these mechanisms are modulated by endogenous nitric oxide (NO). In addition, several humoral factors (such as angiotensin II [Ang II] and prostaglandins [PGs]) play an important role in the control of the tone of these arterioles although their actions are not identical in Af-and Ef-Arts. We found that Ang II caused much stronger constriction in Ef-than in Af-Arts, and that this difference was mediated by the NO-induced modulation of Ang II action in the Af-Art. We have also found that the vasoconstrictor effect of Ang II on Ef-Arts is modulated by PGs produced by the upstream glomerulus. Thus, this may be a mechanism whereby the glomerulus controls its own capillary pressure by releasing PGs, thereby adjusting the resistance of the downstream Ef-Art. Such different mechanisms that regulate Af-and Ef-Art tone play an important role in the precise control of glomerular hemodynamics.

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Renal cortical interstitium and fluid absorption by peritubular capillaries

Cited by 21 publications

References 34 publications

Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis

Proteinuria Triggers Renal Lymphangiogenesis Prior to the Development of Interstitial Fibrosis

Subatmospheric closing pressures in individual microvessels of rats and frogs.

Mechanisms that control glomerular hemodynamics

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