Tubuloglomerular Feedback

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Scott C. Thomson - One of the best experts on this subject based on the ideXlab platform.

Roland C. Blantz - One of the best experts on this subject based on the ideXlab platform.

  • Unexpected effect of angiotensin AT1 receptor blockade on Tubuloglomerular Feedback in early subtotal nephrectomy.
    American journal of physiology. Renal physiology, 2009
    Co-Authors: Prabhleen Singh, Roland C. Blantz, Aihua Deng, Scott C. Thomson
    Abstract:

    After subtotal nephrectomy (STN), the remaining nephrons engage in hyperfiltration, which may be facilitated by a reduced sensitivity of the Tubuloglomerular Feedback (TGF) response to increased di...

  • Glomerulotubular Balance, Tubuloglomerular Feedback, and Salt Homeostasis
    Journal of the American Society of Nephrology : JASN, 2008
    Co-Authors: Scott C. Thomson, Roland C. Blantz
    Abstract:

    The homeostasis of NaCl is critical to complex organisms with closed blood systems. Kidneys regulate this salt excretion by modulating the rapport between glomeruli and tubules. The tubules respond to glomeruli with glomerulotubular balance, whereas glomeruli respond to tubules through Tubuloglomerular Feedback. These relationships are dynamic, mysterious, and amenable to mathematical analyses. The biology underlining what is known about these interactions is observational, fragmentary, and somewhat inconclusive. Discussed here is a simple tethering of these interrelated concepts.

  • Tubuloglomerular Feedback responses of the downstream efferent resistance: unmasking a role for adenosine?
    Kidney international, 2007
    Co-Authors: Roland C. Blantz, Volker Vallon
    Abstract:

    This Commentary aims to integrate or interrelate the available in vivo data with the in vitro study by Ren and co-workers, which comes to the somewhat surprising conclusion that Tubuloglomerular Feedback activation vasodilates the efferent arteriole by an adenosine-dependent mechanism.

  • Regulation of ecto-5'-nucleotidase by NaCl and nitric oxide: potential roles in Tubuloglomerular Feedback and adaptation.
    American journal of physiology. Renal physiology, 2006
    Co-Authors: Joseph Satriano, Scott C. Thomson, Aihua Deng, Lucinda M. Wead, Anna Cardus, Gerry R. Boss, Roland C. Blantz
    Abstract:

    The Tubuloglomerular Feedback (TGF) system serves to establish an appropriate balance between tubular reabsorption and glomerular filtration rate (GFR). High salt at the macula densa activates TGF ...

  • temporal adaptation of Tubuloglomerular Feedback effects of cox 2
    Kidney International, 2004
    Co-Authors: Aihua Deng, Roland C. Blantz, Lucinda M. Wead
    Abstract:

    Temporal adaptation of Tubuloglomerular Feedback: Effects of COX-2. Background Reductions in proximal reabsorption cause increases in delivery of sodium chloride to the macula densa (MD), which activates the Tubuloglomerular Feedback (TGF) mechanism and reduces glomerular filtration rate. TGF undergoes temporal adaptation, permitting filtration rate to rise in spite of elevated MD delivery of NaCl. Inhibitors of nitric oxide synthase I (NOS I) prevent TGF adaptation, but angiotensin-converting enzyme inhibitors have no effect. COX-2 activity moves in parallel with changes in NOS I and intrarenal renin. We examined the impact of COX-2 inhibition on TGF temporal adaptation and effects of inhibition of COX-2 and NOS I on plasma and kidney angiotensin II (Ang II). Methods Kidney blood flow (RBF) and glomerular filtration rate (GFR) were measured before and during benzolamide (BNZ) infusion in control Wistar rats and rats concurrently receiving COX-2 inhibitors. Plasma and kidney angiotensin II content was evaluated by radioimmunoassay in control rats, rats after 60 minutes of BNZ, and during COX-2 and NOS-1 inhibition after BNZ. Results BNZ reduced both RBF and GFR in all groups. During BNZ, RBF and GFR returned to normal control values within 60 minutes. COX-2 inhibitors totally prevented TGF adaptation. Plasma and kidney Ang II did not change after BNZ, and NOS I and COX-2 inhibitors had no effect on plasma or intrarenal Ang II. Conclusion Within 1 hour after BNZ, rats undergo TGF temporal adaptation. Administration of COX-2 inhibitors prevented TGF temporal adaptation, identical to the effect of NOS I inhibition. Changes in intrarenal Ang II cannot explain this prevention of TGF temporal adaptation.

Volker Vallon - One of the best experts on this subject based on the ideXlab platform.

  • Tubuloglomerular Feedback responses of the downstream efferent resistance: unmasking a role for adenosine?
    Kidney international, 2007
    Co-Authors: Roland C. Blantz, Volker Vallon
    Abstract:

    This Commentary aims to integrate or interrelate the available in vivo data with the in vitro study by Ren and co-workers, which comes to the somewhat surprising conclusion that Tubuloglomerular Feedback activation vasodilates the efferent arteriole by an adenosine-dependent mechanism.

  • Tubuloglomerular Feedback and the control of glomerular filtration rate
    Physiology, 2003
    Co-Authors: Volker Vallon
    Abstract:

    In every nephron the glomerular filtration rate is adapted to changes in the salt concentration of early distal tubular fluid through the mechanism of Tubuloglomerular Feedback. Recent studies indicate that adenosine and possibly ATP mediate this mechanism and demonstrate its role in glomerular hemodynamic alterations in the early diabetic kidney.

  • Resetting protects efficiency of Tubuloglomerular Feedback
    Kidney International, 1998
    Co-Authors: Scott C. Thomson, Volker Vallon, Roland C. Blantz
    Abstract:

    Resetting protects efficiency of Tubuloglomerular Feedback. Tubuloglomerular Feedback (TGF) may effect long-term protection of total body salt and water or may govern minute-to-minute autoregulation of renal function. The task for which TGF is best suited depends on the orientation of ambient tubular flow relative to the inflection point of the TGF curve and on the tendency of TGF to reset in response to prolonged stimulation. Current data suggest that the TGF curve is coupled closely to ambient flow in individual nephrons such that the system is capable of compensating both negative and positive perturbations in tubular flow. This coupling is mediated by events within the juxtaglomerular apparatus that cause the TGF curve to reset laterally in response to sustained shifts in tubular flow. This resetting of TGF occurs within 30 to 60minutes of an applied stimulus, suggesting that TGF is better suited to mediate dynamic autoregulation than to account for sustained vasoconstriction during proximal tubular injury.

  • Luminal signal in Tubuloglomerular Feedback: What about potassium?
    Kidney International, 1998
    Co-Authors: Volker Vallon, Roland C. Blantz, Hartmut Osswald, Scott C. Thomson
    Abstract:

    Luminal signal in Tubuloglomerular Feedback: What about potassium? Evidence suggests that a minimal luminal [K+] is required to elicit a full Tubuloglomerular Feedback (TGF) response, consistent with transmission of the TGF signal across the macula densa (MD) via the Na+-2Cl--K+ cotransporter. Furthermore, it appears that luminal [K+] at the MD is close to the K+ affinity of the Na+-2Cl--K+ cotransporter and changes in response to altering late proximal tubular flow rate (VLP), that is, a maneuver that induces a TGF response. These findings suggest that luminal [K+] (besides [Cl-]) could be rate limiting in TGF. In the thick ascending limb of Henle's loop (TALH), most of the luminal K+ is derived from recycling across the apical tubular membrane. Because changing VLP causes relatively greater alterations in the absolute Na+ and Cl- delivery to Henle's loop than in K+ load, the parallel changes of VLP and luminal [K+] at the MD, despite significant alteration in K+-dependent reabsorption of Na+ and Cl- via the Na+-2Cl--K+ cotransporter, imply a transport-dependent adaptation of K+ recycling in TALH.

  • Tubuloglomerular Feedback and its role in acute renal failure
    Critical Care Nephrology, 1998
    Co-Authors: Hartmut Osswald, Volker Vallon
    Abstract:

    The pathophysiology of acute renal failure (ARF) is complex and multifactional. Comprehensive reviews of the current state of knowledge about the different elements of ARF have been published [1, 2]. This chapter will focus on one aspect of ARF that is associated with the physiological mechanism of glomerular filtrate rate (GFR) regulation, i.e., Tubuloglomerular Feedback (TGF). New therapeutic options may result from a better understanding of the pathophysiology of ARF, including possible preventive measures. Reduction of TGF activity is one of the elements that can lead to amelioration of renal impairment and improved clinical outcome in ARF.

A. E. G. Persson - One of the best experts on this subject based on the ideXlab platform.

William J. Welch - One of the best experts on this subject based on the ideXlab platform.

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