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Glomerulotubular Balance, Tubuloglomerular Feedback, and Salt Homeostasis

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Glomerulotubular Balance, Tubuloglomerular Feedback, and Salt Homeostasis SCIENCE IN RENAL MEDICINE www.jasn.org Glomerulotubular Balance, Tubuloglomerular Feedback, and Salt Homeostasis Scott C. Thomson and Roland C. Blantz Department of Medicine, Division of Nephrology-Hypertension, University of California San Diego, and VA San Diego Healthcare System, San Diego, California ABSTRACT The homeostasis of NaCl is critical to complex organisms with closed blood vates apical co-transporters.2 In the loop systems. Kidneys regulate this salt excretion by modulating the rapport between of Henle, GTB is expected to result from glomeruli and tubules. The tubules respond to glomeruli with glomerulotubular the relatively low affinity of the bumet- balance, whereas glomeruli respond to tubules through tubuloglomerular feed- anide-sensitive salt transporter for chlo- back. These relationships are dynamic, mysterious, and amenable to mathematical ride; however, our arguments here rely analyses. The biology underlining what is known about these interactions is obser- only on the existence and inherent limi- vational, fragmentary, and somewhat inconclusive. Discussed here is a simple tations of GTB, which are deduced inde- tethering of these interrelated concepts. pendent of present or future knowledge of its mechanisms. J Am Soc Nephrol 19: 2272–2275, 2008. doi: 10.1681/ASN.2007121326 The inherent limitation of GTB also does not apply to tubular effects of “natri- tropic” nerves and hormones regulating We discuss here the relationship among being reabsorbed. From this we deduce the total body salt through negative feed- glomerulotubular balance (GTB), tubu- the most perfect GTB can do no better back. Instead, the natritropes, which in- loglomerular feedback (TGF), and NaCl than maintain a constant fractional reab- clude angiotensin, aldosterone, natriuretic (salt) handling by the kidney. GTB refers sorption. In reality, GTB in the proximal peptides, and renal nerves, are constrained to the direct positive effect of tubular tubule is approximately 70% efficient at by the immutable requirement for salt bal- flow rate on tubular reabsorption. TGF holding fractional reabsorption con- ance to nullify any long-term disparity be- operates in the juxtaglomerular appara- stant.1 To put this in context, if a person tween salt intake and salt excretion. This tus and confers an inverse dependence of in balance on a 180 mEq/d sodium intake requirement is immutable because the al- single-nephron GFR on tubular fluid salt with GFR 180 L/d and fractional reab- ternative advances an untenable notion of reaching the macula densa. GTB and sorption of 80% up to the macula densa infinite total body salt. TGF form a negative feedback system were to experience a 10% increase in that stabilizes both single-nephron GFR GFR, then 44% of the increment in fil- and distal salt delivery. Most of our tered load would arrive at the macula COMBINING GTB WITH TGF points are made by deduction. densa. GTB downstream from the mac- ula densa is difficult to quantify, but as- Because of the limitations of GTB, a por- suming constant fractional reabsorption tion of any change in GFR will pass along EXISTENCE AND LIMITATIONS OF (to wit perfect distal GTB), this 10% in- the nephron to elicit a TGF response, GTB crease in GFR would effect a 22% in- which will offset part of the original dis- crease in salt excretion. turbance. The uncompensated portion Tubular reabsorption is a random pro- The mechanisms of GTB have been cess, subject to statistical laws. Accord- argued since the 1930s and are not en- Published online ahead of print. Publication date ingly, more delivery translates to more tirely clear, even today. GTB depends available at www.jasn.org. chances for reabsorption, which trans- partly on parallel changes in peritubular Correspondence: Dr. Scott C. Thomson, Depart- lates to more total reabsorption. Ergo, capillary oncotic pressure that accom- ment of Medicine, University of California, and VA San Diego Healthcare System, 3350 La Jolla Village Drive GTB exists. But increasing the flow pany changes in filtration fraction. Re- 9111H, San Diego, CA 92161. Phone: 858-552-7528; through a nephron segment also in- cently, a luminal mechanism has also Fax: 858-552-7549; E-mail: [email protected] creases the opportunity for an individual been identified in which shear strain on Copyright ᮊ 2008 by the American Society of molecule to transit the segment without the proximal tubule brush border acti- Nephrology 2272 ISSN : 1046-6673/1912-2272 J Am Soc Nephrol 19: 2272–2275, 2008 www.jasn.org SCIENCE IN RENAL MEDICINE of the original disturbance remains as an sudden change in total body salt. In ad- in distal delivery disruptive. Further- error signal. The ratio of the compensa- dition, this construct provides a fair lit- more, not all changes in salt delivery to tion to the error signal is termed the open eral representation, because activation of the macula densa help to stabilize total loop gain (OLG). The OLG of any feed- the major natritropes is tied to changes in body salt. For example, if GFR, hence back loop equals the product of the the total body salt. The natritropic hor- macula densa salt, were passively allowed slopes of its pair-wise relations (see Ap- mones and nerves make for a more stable to track short-term fluctuations in BP pendix). Typically, the negative OLG for total body salt, but, to the extent that they that occur independent of total body salt, the GTB-TGF system is approximately 2, act by changing GFR or proximal reab- then fluctuating salt excretion would fol- which means that the system compen- sorption, their effectiveness is attenuated low, irrespective of total body salt. Or if sates for approximately 66% of an out- by TGF. In other words, when the object proximal reabsorption were to decline in side disturbance,3 so an outside distur- of homeostasis is the total body salt, TGF the aftermath of some injury to the tu- bance that would increase GFR by 10% is antihomeostatic. bule, then macula densa salt would in- and salt excretion by 22% in the absence This, too, can be deduced: Any change crease independent of total body salt. of TGF winds up as a 3% increase in GFR in salt excretion equals a change in deliv- The kidney invokes TGF to lessen the im- and a 7% increase in salt excretion. Cur- ery to the macula densa minus a change pact of such transient events on GFR and rent thinking on the mechanism of TGF in reabsorption downstream from the salt excretion,6 but this inevitably re- is that the macula densa releases ATP in macula densa. Hence, there is potential quires some sacrifice of salt homeostasis. proportion to the tubular fluid salt con- for natritropes to speed up the salt bal- The relative contribution of proximal centration and this ATP binds to vaso- ance by impinging both upstream and and distal nephrons to overall salt bal- constrictor purinergic receptors on the downstream from the macula densa. But ance must vary according to the relative afferent arteriole and/or converts to TGF makes the distal delivery resistant to OLG of the GTB-TGF and natritropic adenosine, which activates vasoconstric- change. If GTB-TGF were perfectly effi- feedback systems. A model for this is de- tor adenosine A1 receptors on afferent cient (OLG infinite), then total responsi- veloped in the Appendix. When num- arterioles. The sensitivity of this feedback bility for salt balance would be relegated bers derived from the published litera- is susceptible to modulation by a variety downstream from the macula densa. ture are applied to this model, it is of mediators, including nitric oxide, This competition between TGF and the revealed that eliminating TGF would prostaglandins, and angiotensin II, natritropes results in a compromise be- lessen by 30% the impact of dietary salt among others.4 tween the efficient compensation for on the total body salt. changes in salt intake and control of the distal salt delivery. The integration of this GTB, TGF, AND SALT compromise is inherent and its details TGF ADAPTATION: LIMITING THE HOMEOSTASIS are revealed by solving a simple system of COST OF TGF equations developed from the individual After a change in salt intake, salt excre- pair-wise relations between total body Because of the inverse relationship im- tion asymptotically catches up to the new salt, the natritropes, and their effects on posed by TGF, glomerular filtration and intake and balance is restored at a new the various nephron segments (see Ap- distal salt delivery cannot change in the total body salt. Over time, total body salt pendix). same direction unless there is resetting of varies directly with the salt intake, and the TGF curve. For example, acute the slope of this relationship is inversely plasma volume expansion, which in- related to how rapidly balance is restored ADVANTAGES TO creases both GFR and distal delivery, after a change in salt intake. When bal- COMPROMISING ON THE must cause rightward resetting of TGF.3 ance is restored rapidly, the total body EFFICIENCY OF SALT Furthermore, the natural tendency for salt is less sensitive to long-term salt in- HOMEOSTASIS tubular flow to align with the steepest take than when balance is restored part of the TGF curve suggests resetting slowly, so the efficiency of salt homeosta- A stable internal environment is essential at the level of each nephron, a phenom- sis boils down to how long it takes to re- for normal functioning of the organs, so enon that has been confirmed.7,8 If TGF store balance after a change in salt intake. why incorporate TGF, which naturally resets rightward during prolonged acti- The most parsimonious explanation for lessens the efficiency of sodium ho- vation, then this will lessen its apparent observed behavior is a system in which meostasis? Sodium is not the only im- OLG for buffering long-term (hours/ salt excretion is driven not by salt intake portant constituent of the body fluids.
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