The Juxtaglomerular Apparatus

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The need for autoregulation of the glomerular filtration rate is apparent. If the flow rate of filtrate is too slow, then we expect reabsorption to be too high, and the kidney fails to eliminate necessary waste products. On the other hand, at too high a flow rate, the tubules are unable to reabsorb those substances that need to be preserved and not eliminated, so that valuable substances are lost into the urine.

The idea of how to regulate the flow of filtrate is simple to understand. If you had a leaky hose and wanted to control the leakage rate precisely, regardless of the total flow

Action Potentials Filtration

Figure 20.4 Unregulated glomerular filtration and renal blood flow plotted as functions of arterial pressure, with Pd = 18, Pe = 0 mm Hg.

Arterial pressure (mm Hg)

Figure 20.4 Unregulated glomerular filtration and renal blood flow plotted as functions of arterial pressure, with Pd = 18, Pe = 0 mm Hg.

Autoregulation Renal Blood Flow

Figure 20.5 Autoregulation of renal blood flow and glomerular filtration rate but lack of autoregulation of urine flow during changes in renal arterial pressure. (Guyton and Hall, 1996, Fig. 26-13, p. 327.)

Arterial pressure (mm Hg)

Figure 20.5 Autoregulation of renal blood flow and glomerular filtration rate but lack of autoregulation of urine flow during changes in renal arterial pressure. (Guyton and Hall, 1996, Fig. 26-13, p. 327.)

rate, you could do so by regulating the outflow pressure at the end of the hose. The way the glomerulus controls the rate of filtration is similar. After its descent into the renal medulla, the long tubule returns to the proximity of the afferent and efferent arterioles at the glomerulus. The juxtaglomerular complex consists of macula densa cells in the

Complex Juxtaglomerular Apparatus
Figure 20.6 Structure of the juxtaglomerular apparatus. (Guyton and Hall, 1996, Fig. 26-14, p. 328.)

distal tubule and juxtaglomerular cells in the walls of the afferent and efferent arterioles (as depicted in Fig. 20.6).

A low flow rate causes excessive reabsorption of Na+ and chloride ions in the ascending limb of the loop of Henle, resulting in too large a decrease of these ionic concentrations at the end of the loop. The macula densa cells respond to decreases of Na+ concentration (by a mechanism not completely understood), by releasing a vasodilator that decreases the resistance of the afferent arterioles. Simultaneously, the juxtaglomerular cells release renin, an enzyme that enables the formation of angiotensin II, which constricts the efferent arterioles. The simultaneous effect of these is to increase the flow of filtrate through the glomerulus.

A simple model to incorporate the effects of the vasodilator and vasoconstrictor (angiotensin) is to allow the arteriole resistances to depend on the rate of filtration, Qd = Qi — Qe, via some functional dependence

where Qt is the target flow rate, about 125 ml/min. A more realistic model would take Ra and Re to be functions of the Na+ concentration at the distal end of the loop of Henle. However, since we do not yet have a model relating flow rate to Na+ concentration, we leave this to interested readers to pursue on their own.

We take fa to be an increasing function of its argument, and we take fe to be a decreasing function of its argument. As a specific example, we take

Ra = Tail + tanh(5fl(Qd - Q,))], Re = Teil - tanh(Se(Qd - Qt))],

where Sa and Se are parameters that determine the sensitivity of the model to changes in flow rates, and ra and re are "normal" values of the resistances. With Sa and Se zero, the flow is unregulated. There is no direct evidence for these functional forms, so these results are qualitative at best. Plots of the functions Ra/ra and Re/re are shown in Fig. 20.7, with 8a = 0-1, 8e = 0-01, Qt = 125 ml/min. With these parameters, control of afferent resistance is stronger than that of efferent resistance.

In Fig. 20.8 are shown the glomerular filtration and the renal blood flow as functions of the arterial pressure, in the case 8a = 0-1, 8e = 0-01. This simple model gives accept-

Juxtaglomerular Apparatus Model

60 80 100 120 140 160 180 Arterial pressure (mm Hg)

60 80 100 120 140 160 180 Arterial pressure (mm Hg)

Figure 20.7 Relative resistances Ra/ra and Re/re plotted as functions of glomerular flow rate Qd with 8a = 0.1, 8e = 0.01, qt = 125 ml/min.

Action Potentials Filtration

Figure 20.8 Autoregulated glomerular filtration flow rate and renal blood flow rate, with 8a = 0.1, 8e = 0.01, Qt = 125 ml/min, and with Pd = 18, Pe = 0 mm Hg.

60 80 100 120 140 160 180 200 Arterial pressure (mm Hg)

60 80 100 120 140 160 180 200 Arterial pressure (mm Hg)

Figure 20.8 Autoregulated glomerular filtration flow rate and renal blood flow rate, with 8a = 0.1, 8e = 0.01, Qt = 125 ml/min, and with Pd = 18, Pe = 0 mm Hg.

able agreement with data, although there was no attempt to find a good quantitative fit.

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  • lukas
    How does the juxtaglomerular complex respond to decreases in the filtration pressure?
    6 years ago

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