Porth's Essentials of Pathophysiology, 4e

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Kidney and Urinary Tract Function

U N I T 7

Two major systems are credited with maintaining the constancy of renal blood flow and GFR: one responds to changes in arterial pressure and the other to changes in the sodium chloride concentration in the distal tubu- lar fluid. Both serve to regulate the tone of the afferent arteriole. The pressure sensitive mechanism, termed the myogenic mechanism , relies on the intrinsic property of vascular smooth muscle that causes it to contract when stretched. Thus, when the arterial pressure rises and the afferent arteriole is stretched, the smooth mus- cle contracts; when arterial pressure falls, the smooth muscle relaxes. The second mechanism, termed the tubuloglomerular feedback mechanism, involves a feedback loop in which the sodium chloride concentration in the tubular fluid is sensed by the juxtaglomerular apparatus (“juxta” meaning “next to”) in the distal tubule. This feedback system, which is located at the site where the distal tubule extends back to the glomerulus and then passes between the afferent and efferent arterioles, includes a group of sodium sensing cells called the macula densa and special secretory cells in the walls of afferent and efferent arterioles called juxtaglomerular cells that syn- thesize and release the enzyme renin (Fig. 24-11A). Because of its location between the afferent and effer- ent arterioles, the juxtaglomerular apparatus is thought to play an essential feedback role in linking the level of arterial blood pressure and renal blood flow to the GFR and the composition of the distal tubular fluid (see Fig. 24-11B). It is thought to monitor the arterial

blood pressure by sensing both the stretch of the affer- ent arteriole and the concentration of sodium chloride in the tubular filtrate as it passes through the macula densa. This information is then used in determining how much renin should be released to keep the arterial blood pressure within its normal range and maintain a rela- tively constant GFR. A decrease in the GFR, for exam- ple, increases sodium chloride reabsorption, thereby decreasing the delivery of sodium chloride to the macula densa. The decrease in delivery of sodium chloride to the macula densa has two effects: it decreases resistance to blood flow in the afferent arteriole, which raises glo- merular filtration pressure; and it increases the release of renin from the juxtaglomerular cells. The renin from these cells functions as an enzyme to convert the plasma protein angiotensinogen to angiotensin I, which is con- verted to angiotensin II in the lungs (see Chapter 18, Fig. 18-12). Angiotensin II acts to constrict the efferent arteriole as a means of producing a further increase in the glomerular filtration pressure; thereby returning the GFR toward a more normal range. Effects of Increased Protein and Glucose Load Although renal blood flow and glomerular filtration are relatively stable under most conditions, two factors can increase renal blood flow and glomerular filtration: (1) high protein intake, (2) an increase in blood glu- cose. With ingestion of a high-protein meal, renal blood flow increases 20% to 30% within 1 to 2 hours.

Arterial pressure

Glomerular hydrostatic pressure

Basement membrane

GFR

Juxtaglomerular cells

Proximal NaCl reabsorption

Glomerulus

Macula densa NaCl

Renin

Afferent arteriole

Angiotensin II

Efferent arteriolar resistance

Afferent arteriolar resistance

Macula densa

Efferent arteriole

Distal tubule

A

B

FIGURE 24-11. (A) Juxtaglomerular apparatus showing the close contact of the distal tubule with the afferent arteriole, the macula densa, and the juxtaglomerular cells. (B) Flow chart depicting the macula densa feedback mechanism for autoregulation of glomerular hydrostatic pressure and glomerular filtration rate (GFR) during changes in renal arterial pressure. (From Hall JE. Guyton and HallTextbook of Medical Physiology. 12th ed. Philadelphia, PA: Saunders Elsevier; 2011:320.)