A. The kidney is able to maintain both RBF and GFR relatively constant in the face of changes in arterial pressure from about 80 to 200 mm Hg in the absence of changes in sympathetic neural input and in circulating levels of vasoactive substances (Fig. 2-10). Below that range changes in arterial pressure may have large effects on RBF and GFR. The fact that GFR is maintained constant indicates that P_gc, as well as glomerular plasma flow, is kept constant. It is apparent then, that resistance upstream from the glomerular capillaries in the afferent arteriole must change as renal artery pressure changes. Efferent arteriolar resistance may change also, but it is obvious that the major change occurs in the afferent arteriole.

Fig. 2-10. Autoregulation. The effect of changes in arterial pressure on RBF and GFR.

1. The smooth muscle within the walls of the arterioles respond directly to the stretching effect of a rise in pressure within the arteriole by increasing the contraction of their smooth muscle cells, thereby reducing the diameter of the arteriole and increasing its resistance to flow. This is called the intrinsic myogenic response.

2. The TGF mechanism involves the juxtaglomerular apparatus and the close anatomical relationship among the macula densa, the glomerulus and the arterioles of the same nephron (Fig 2-11). The macula densa senses changes in the composition of tubular fluid that occur when the tubular fluid flow rate changes and signals the afferent arteriole to alter constriction. Changes in the tubular fluid flow rate are brought about by changes in GFR and/or the rate of reabsorption in the proximal tubule. For example a rise in GFR increases the tubular fluid flow rate at the macula densa. That triggers an increase in afferent arteriolar resistance that reduces pressure in the glomerular capillaries and brings GFR back down. The rise in resistance also reduces RBF.

Fig. 2-11. The tubuloglomerular feedback mechanism.

3. The macula densa apparently senses changes in the delivery of Cl^- ([Cl] in tubular fluid x tubular fluid flow rate) that occur as flow rate changes. The macula densa cells absorb Cl^- and the rate of reabsorption is dependent on the rate of delivery. It is thought that an increase in reabsorption causes the release of a paracrine, perhaps adenosine, that causes the afferent arteriolar smooth muscle cells to contract.

C. Both the myogenic mechanism and the TGF mechanism contribute to autoregulation but the extent of the participation of each and how each responds to various situations that alter RBF and GFR is still largely unknown.

QUESTIONS:  
17. In the absence of changes in extrinsic factors, the kidney autoregulates RBF and GFR. To regulate both it seems obvious that the major change in resistance must occur in which arteriole? Why?

18. On what primary anatomical feature is the tubuloglomerular feedback mechanism based? What does this mechanism primarily regulate, GFR or RPF? In this feedback mechanism, what is the signal, the sensor, the effector?

19. Considering the TGF mechanism, what would be the effect on GFR of a fall in the rate of fluid reabsorption in the proximal tubule?

20. What other mechanism may be invoved in autoregulation? How would this mechanism respond to maintain GFR and RPF constant when arterial blood pressure is increased?

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