Arterioles afferent

The kidney contains the major site of renin synthesis, the juxtaglomerular cells in the wall of the afferent arteriole. From these cells, renin is secreted not only into the circulation but also into the renal interstitium. Moreover, the enzyme is produced albeit in low amounts by proximal tubular cells. These cells also synthesize angiotensinogen and ACE. The RAS proteins interact in the renal interstitium and in the proximal tubular lumen to synthesize angiotensin II. In the proximal tubule, angiotensin II activates the sodium/hydrogen exchanger (NHE) that increases sodium reabsorption. Aldosterone elicits the same effect in the distal tubule by activating epithelial sodium channels (ENaC) and the sodium-potassium-ATPase. Thereby, it also induces water reabsotption and potassium secretion. 

Explain how sympathetic nerves, angiotensin II, and prostaglandins affect the resistance of the afferent arteriole... 

Figure 19.1 The nephron. The functional unit of the kidney is the nephron, which has two components. The vascular component includes the afferent arteriole, which carries blood toward the glomerulus where filtration of the plasma takes place. The efferent arteriole carries the unfiltered blood away from the glomerulus. The tubular component of the nephron includes Bowman s capsule, which receives the filtrate the proximal tubule the Loop of Henle and the distal tubule. The tubule processes the filtrate, excreting waste products and reabsorbing nutrient molecules, electrolytes, and water.

Glomerular capillary pressure is determined primarily by renal blood flow (RBF). As RBF increases, PGC and therefore GFR increase. On the other hand, as RBF decreases, PGC and GFR decrease. Renal blood flow is determined by mean arterial pressure (MAP) and the resistance of the afferent arteriole (aff art) ... 

Myogenic mechanism. As discussed in Chapter 16 on the circulatory system, the myogenic mechanism involves contraction of vascular smooth muscle in response to stretch. For example, an increase in MAP would tend to increase RBF, leading to an increase in pressure within the afferent arteriole and distension, or stretch, of the vessel wall. Consequently, the vascular smooth muscle of the afferent arteriole contracts, increases the resistance of the vessel, and decreases RBF toward normal. 

An increase in MAP leads to an increase in RBF, PGC/ and GFR. As a result, the rate of fluid flow through the distal tubule increases, leading to an increase in reabsorption of Na+ and Cl ions by the cells of the macula densa in the distal tubule. Consequently, these cells release vasoconstrictor substances, primarily adenosine. The subsequent increase in the resistance of the nearby afferent arteriole decreases RBF to normal and, as a result, PGC and therefore GFR decrease to normal. In this way, the distal tubule regulates its own filtrate flow. 

Resistance of the afferent arteriole. Many physiological conditions warrant a change in RBF and GFR, even when MAP is within the autoregulatory range. For example, volume overload is resolved with an increase in RBF, GFR, and urine output so that excess water and solutes are eliminated. Conversely, volume depletion, such as that which occurs with hemorrhage or dehydration, is resolved with decreased RBF, GFR, and urine output in this way, water and solutes are conserved. 

The resistance of the afferent arteriole is influenced by several factors, including (see Table 19.1) ... 

Sympathetic nerves. The afferent and efferent arterioles are densely innervated with sympathetic nerves. Norepinephrine released directly from the nerves or circulating epinephrine released from the adrenal medulla stimulates a, adrenergic receptors to cause vasoconstriction. The predominant site of regulation is the afferent arteriole. Under normal resting conditions, there is little sympathetic tone to these vessels so that RBF is comparatively high. As discussed previously, this facilitates glomerular filtration. 

An overall increase in sympathetic nerve activity includes an increase in sympathetic input to the kidneys. Consequently, resistance of the afferent arteriole increases, leading to a decrease in RBF. As discussed, this results in a decrease in PGC, GFR, and urine output. As such, the renal excretion of sodium and water is decreased. In other words, sodium and water are... 

The granular cells that secrete renin also serve as intrarenal baroreceptors, monitoring blood volume and blood pressure in the afferent arterioles. Arteriolar pressure and renin secretion have an inverse relationship in other words, an increase in blood volume causes an increase in arteriolar blood pressure increased stimulation of the intrarenal baroreceptors and decreased secretion of renin. With less angiotensin Il-induced vasoconstriction of the afferent arteriole, RBF, GFR, and urine output will increase so that blood volume returns to normal. 

T Resistance of afferent arteriole —> 4 renal blood flow — 4 glomerular filtration rate -4 4 Na+ filtration... 

Sodium is freely filtered at the glomerulus. Therefore, any factor that affects GFR will also affect sodium filtration. As discussed previously, GFR is directly related to RBF. In turn, RBF is determined by blood pressure and the resistance of the afferent arteriole (RBF = AP/R). For example, an increase in blood pressure or a decrease in resistance of the afferent arteriole will increase RBF, GFR, and, consequently, filtration of sodium. The amount of sodium reabsorbed from the tubules is physiologically regulated, primarily by aldosterone and, to a lesser extent, by ANP. Aldosterone promotes reabsorption and ANP inhibits it. The alterations in sodium filtration and sodium reabsorption in response to decreased plasma volume are illustrated in Figure 19.6. 

Widespread vasoconstriction supplements the increase in TPR induced by the sympathetic nervous system. Angiotensin II also causes vasoconstriction of the afferent arteriole in particular, which enhances the decrease in RBF and sodium filtration. Finally, angiotensin II promotes secretion of aldosterone from the adrenal cortex. Aldosterone then acts on the distal tubule and collecting duct to increase sodium reabsorption. 

Kidneys are exquisitely sensitive to changes in perfusion pressures. Moderate alterations can lead to significant changes in glomerular filtration rate. Oliguria, progressing to anuria, occurs because of vasoconstriction of afferent arterioles. 

Three generally accepted mechanisms are involved in the regulation of renin secretion (Fig. 18.2). The first depends on renal afferent arterioles that act as stretch receptors or baroreceptors. Increased intravascular pressure and increased volume in the afferent arteriole inhibits the release of renin. The second mechanism is the result of changes in the amount of filtered sodium that reaches the macula densa of the distal tubule. Plasma renin activity correlates inversely with dietary sodium intake. The third renin secretory control mechanism is neurogenic and involves the dense sympathetic... 

Increased pressure in afferent arteriole leads to decreased renin release by JG cells. 

The renal vascular receptor functions as a stretch receptor, with decreased stretch leading to increased renin release and vice versa. The receptor is apparently located in the afferent arteriole, possibly in the juxtaglomerular cells. Stretch-induced changes in renin release are mediated by changes in Ca2+ concentration in the juxtaglomerular cells. 

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