When there is a decrease in renal perfusion, the glomerular filtration rate (GFR) also decreases due to a fall in the glomerular capillary pressure (PGC). This decrease in PGC can be caused by a decline in renal arterial pressure, an increase in afferent arteriolar resistance, or a decrease in efferent arteriolar resistance.

There is an inverse relationship between the glomerular colloid osmotic pressure (πGC) and GFR. Changes in πGC are a result of alterations in protein synthesis outside the kidneys. Additionally, renal diseases that cause protein loss in urine can lead to a decrease in plasma protein concentration and therefore in πGC.

The effective filtration pressure (PBS) plays a role in GFR. An increase in PBS reduces GFR, while a decrease in PBS enhances GFR. Acute obstruction of the urinary tract, such as a kidney stone occluding the ureter, leads to an increase in PBS.

The resistance to flow through the kidneys, denoted by organ R, can be calculated using the equation RBF = (renal artery pressure - renal vein pressure) / renal vascular resistance.

The major resistance vessels in the kidneys are the afferent arteriole, efferent arteriole, and interlobular artery. These vessels determine the renal vascular resistance and, like other organs, the kidneys regulate their blood flow by adjusting vascular resistance in response to changes in arterial pressure. This regulation ensures that blood flow and GFR remain relatively constant within a range of arterial pressures (90-180 mm Hg), as shown in Figure 33.18. Autoregulation, the phenomenon responsible for maintaining constant RBF and GFR within this range of pressures, primarily involves changes in vascular resistance, mainly through the afferent arterioles. Given the importance of RBF in determining GFR, it is not surprising that the same mechanisms regulate both flows.

Two mechanisms contribute to the autoregulation of RBF and GFR: one responds to changes in arterial pressure, while the other responds to changes in the concentration of sodium chloride (NaCl) in tubular fluid. Both mechanisms regulate the tone of the afferent arteriole. The pressure-sensitive mechanism, known as the myogenic mechanism, is related to the tendency of vascular smooth muscle to contract when stretched. When arterial pressure increases and stretches the renal afferent arteriole, the smooth muscle contracts in response. This contraction increases resistance in the arteriole, offsetting the increase in pressure and maintaining constant RBF and GFR.
Changes in PGC: With decreased renal perfusion, GFR declines because PGC falls. As previously discussed, a reduction in PGC is caused by a decline in renal arterial pressure, an increase in afferent arteriolar resistance, or a decrease in efferent arteriolar resistance.
3.
Changes in πGC: An inverse relationship exists between πGC and GFR. Alterations in πGC result from changes in protein synthesis outside the kidneys. In addition the protein loss in urine caused by some renal diseases can lead to a decrease in the plasma protein concentration and thus in πGC.
4.
Changes in PBS: Increased PBS reduces GFR, whereas decreased PBS enhances GFR. Acute obstruction of the urinary tract (e.g., a kidney stone occluding the ureter) increases PBS.
Equation 33.11 organ R = resistance to flow through that organ
Accordingly, RBF is equal to the pressure difference between the renal artery and the renal vein divided by renal vascular resistance:
Equation 33.12
The afferent arteriole, efferent arteriole, and interlobular artery are the major resistance vessels in the kidneys and thereby determine renal vascular resistance. Like most other organs, the kidneys regulate their blood flow by adjusting vascular resistance in response to changes in arterial pressure. As shown in
Fig. 33.18 these adjustments are so precise that blood flow remains relatively constant as arterial blood pressure changes between 90 and 180 mm Hg. GFR is also regulated over the same range of arterial pressures. The phenomenon whereby RBF and GFR are maintained relatively constant between blood pressures of 90 and 180 mm Hg, namely autoregulation, is achieved by changes in vascular resistance, mainly through the afferent arterioles of the kidneys. Because both RBF and GFR are regulated over the • Fig. 33.18 Relationship between arterial blood pressure and RBF and between arterial blood pressure and GFR. Autoregulation maintains GFR and RBF relatively constant as blood pressure changes from 90 to 180 mm Hg.
same range of pressures and because RBF is an important determinant of GFR, it is not surprising that the same mechanisms regulate both flows.
Two mechanisms are responsible for autoregulation of RBF and GFR: one mechanism that responds to changes in arterial pressure and another that responds to changes in [NaCl] in tubular fluid. Both regulate the tone of the afferent arteriole. The pressure-sensitive mechanism, the so-called myogenic mechanism, is related to an intrinsic property of vascular smooth muscle: the tendency to contract when stretched. Accordingly, when arterial pressure rises and the renal afferent arteriole is stretched, the smooth muscle contracts in response. Because the increase in resistance of the arteriole offsets the increase in pressure, RBF, and therefore GFR, remains constant. (That is, RBF is constant if ΔP/R is kept constant [see
Eq. 33.11