Renal Circulation

Renal circulation essentially refers to the blood flow to the kidneys. Flow to the kidneys is very high, accounting for about 20% (~1.25mL/min) of cardiac output, though it only accounts for .5% of total body weight. The kidneys primary function is to filter the blood, which accomplishes a number them:

Flow into the kidneys begins at the renal artery, branches into the interlobar artery, arcuate artery, interlobular artery, and the afferent arteriole, which leads into the glomerular capillaries. The glomerular capillaries coalesce to form the efferent arteriole, which leads into a second capillary network, the peritubular capillaries. The vessels of the venous system run parallel to the arterial vessels and progressively form the interlobular vein, the arcuate vein, the interlobar vein, and the renal vein.

The afferent arteriole, the efferent arteriole, and the interlobar artery are the major resistance vessels in the kidneys. Blood flow is controlled by adjusting vascular resistance, e.g. vasodilation and vasoconstriction and is maintained at a nearly constant rate by autoregulation for blood pressures changes between 90 and 180mmHg.

Two mechanisms are responsible for autoregulation: one responds to changes in arterial pressure and the other responds to changes in renal tubular flow. The first mechanism via a pressure sensitive myogenic mechanism, which is related to an intrinsic muscle property of vascular smooth muscle, which surrounds the aforementioned vessels: the tendency to contract when stretched. Thus, when arterial pressure rises and the renal afferent arteriole is stretched, the smooth muscles contract. Because the increase in the resistance of the arteriole offsets the increase pressure, blood flow remains constant.

The second mechanism is a flow dependent mechanism known as tubuloglomerular feedback. The mechanism involves a feedback loop in which tubular fluid, which sensed by the macula densa of the juxtaglomerulara apparatus (JGA), near the end of the loop of Henle, and is converted into a signal that affects the glomerular flow rate (GFR). When GFR increases and causes the flow rate of the tubular fluid in the macula densa to rise, the JGA sends a signal that causes GFR and renal blood flow to decrease return to normal. In contrast, when GFR flow decreases, the JGA sends signals to increase GFR and renal blood flow to normal levels. Both normalization methods are accomplished by changing the resistance of afferent neurons.

All in all autoregulation provides an effective means of uncoupling renal function from arterial pressures and ensures that fluid and solute excretion remains constants. 

Renal Blood Flow = ((Aortic Pressure) - (Renal Venous Pressure)) / Renal Vascular Resistance

Sample Problems:

  If Aortic pressure was initially 120mmHg and venous pressure was 90mmHg and resistance was 240, and suddenly aortic pressure jumped to about 170 and venous pressure was constant, how much would the vascular resistance have to change in order to maintain normal renal blood flow.

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This page was written by Hoa T. Le, a student in this course.

BME 403 Pages maintained by the T.A., Douglas Miles.