Send to

Choose Destination
See comment in PubMed Commons below
Acta Physiol Hung. 2007 Mar;94(1-2):83-94.

Coordination of kidney filtration and tubular reabsorption: considerations on the regulation of metabolic demand for tubular reabsorption.

Author information

Division of Nephrology-Hypertension, School of Medicine, University of California, & VASDHS 3350 La Jolla Village Drive (111-H) San Diego, California 92161, USA.


Kidney blood flow is highly regulated by a combination of myogenic autoregulation, multiple neurohormonal systems and the tubuloglomerular feedback system, the later of which specifically relates tubular reabsorption to the filtered load. Oxygen and substrate requirements of the kidney are dictated by both supply of oxygen and substrates and metabolic demands of the kidney. The tubuloglomerular feedback system utilizes mediators which are intimately linked to cellular metabolism, ATP and adenosine. This system based upon communication transfer between the macular densa and the afferent arteriole stabilizes kidney function and is not static but temporally adapts or resets to new external physiologic conditions. Such temporal adaptation occurs via modulators such as nitric oxide (NO), primarily derived from NOS-1, angiotensin II and COX-2 products. These hormonal influences also exert capacities to modulate cellular demands for oxygen, particularly NO which decreases oxygen consumption via multiple mechanisms. The several mechanisms whereby NO and other hormonal systems and transporter activity can regulate and produce changes in kidney metabolic demands are discussed. Modulators which influence temporal adaptation and resetting of TGF are also significant contributors to the regulation of cellular oxygen consumption in the kidney. These systems may act in concert to preserve the coordination of filtered load and tubular reabsorption and the metabolic demands of kidney function, thereby determining the ischemic threshold for kidney function.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Atypon
    Loading ...
    Support Center