Consideration of the forces operating at the glomerular and peritubular capillaries reveals that even relatively small changes in the pressures and flows can cause substantial alterations in filtered and reabsorbed volumes. To minimize the effects of external disturbances such as changes in arterial perfusion pressure, the renal vasculature has powerful mechanisms that maintain a stable intrarenal hemodynamic environment and a controlled filtered load. Through active adjustments of smooth muscle tone of the afferent arterioles, the autoregulatory mechanism helps maintain an optimum filtered load and also provides a reserve capability that can be utilized during pathological processes that compromise renal hemodynamic function [1, 23]. As shown in Fig. 2, both RBF and GFR demonstrate highly efficient autoregulation in response to changes in perfusion pressure. In addition, the intrarenal pressures in the glomerular and peritubular capillaries and in the proximal tubules exhibit autoregulatory behavior. These characteristics of the autoregulatory phenomenon indicate that the major site for autoregulatory resistance adjustments is preglomerular. Direct observations of afferent and efferent arteriolar diameters during changes in perfusion pressure have confirmed this conclusion [25, 36].
Two mechanisms interact to provide highly efficient renal autoregulation: the macula densa feedback mechanism and the myogenic mechanism. The macula densa mechanism, also known as the tubuloglomerular feedback (TGF) mechanism is depicted in Fig. 3. In response to perturbations that increase distal tubular fluid flow past the macula densa, signals are sent to afferent arterioles to elicit vasoconstriction, whereas decreases in flow will cause afferent vasodilation [1, 4, 5, 25, 38, 39]. Micropuncture experiments have shown that o 50 100 150 200
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FIGURE 2. Renal autoregulatory responses to changes in RAP and associated changes in sodium excretion and segmental vascular resistances. The relationship between arterial pressure and sodium excretion is called the pressure natriuresis curve and can be adjusted by the intrarenal hemodynamic and hormonal status. States associated with ECFV expansion increase the slope of the curve, while conditions of dehydration and reduced ECFV will
FIGURE 2. Renal autoregulatory responses to changes in RAP and associated changes in sodium excretion and segmental vascular resistances. The relationship between arterial pressure and sodium excretion is called the pressure natriuresis curve and can be adjusted by the intrarenal hemodynamic and hormonal status. States associated with ECFV expansion increase the slope of the curve, while conditions of dehydration and reduced ECFV will increases in distal volume delivery in a single nephron elicit reductions in single nephron GFR (SNGFR) (Fig. 3), glomerular capillary hydrostatic pressure, and glomerular plasma flow. Furthermore, if there is residual tone in the afferent arterioles, interruption of fluid delivery to the distal nephron increases SNGFR above values obtained under conditions of maintained distal flow. This manipulation opens the feedback loop and attenuates autoregulatory efficiency of SNGFR and glomerular pressure, indicating that an intact TGF mechanism is required for efficient autoregulation. Autoregulatory responses seen at the level of the whole kidney represent one manifestation of this homeostatic mechanism, which maintains a balance between filtered load and the reabsorp-tive capabilities of each nephron.
The myogenic mechanism is based on the premise that preglomerular arterioles can sense changes in vessel wall tension and respond with appropriate adjustments in tone. An increase in wall tension, occurring in response to an elevation in arterial pressure, is thought to stimulate a vascular sensor element and initiate a sequence of events resulting in vascular smooth muscle contraction. Interlobular and arcuate arteries and afferent arterioles, but not efferent arterioles, exhibit myogenic responses to changes in wall tension. The residual autoregulatory capacity that exists during blockade of the tubuloglomerular feedback mechanism indicates that the myogenic mechanism contributes to autoregulatory responses of the renal vasculature [1, 25].
Autoregulatory behavior has been demonstrated in all regions of the kidney. Both cortical and juxtamedullary nephrons have a highly sensitive TGF mechanism, and deep nephrons autoregulate as efficiently as superficial nephrons. Since the medullary circulation is primarily a postglomerular circuit, its response should be similar to that of inner cortical nephrons. Although studies in rats indicate that medullary blood flow is less well autoregulated then cortical blood flow , studies in dogs have documented highly efficient autoregulation of the medullary circulation . Under most circumstances the autoregulatory mechanism serves a critical function to stabilize the micro-circulatory environment throughout the kidney.
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