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' Na* reabsorption ■ Extracellular fluid volume 1 K* secretion

FIGURE 9 Production of angiotensin II by the release of renin from juxtaglomerular cells. A variety of signals associated with falling blood pressure and/or extracellular fluid volume loss cause release of renin from juxtaglomerular cells. Renin acts as an enzyme to cleave angiotensin I from an a2-globulin, angiotensinogen. Angiotensin I is changed to angiotensin II by the cleavage of two amino acids, a process catalyzed by ACE. Angiotensin II acts on vascular smooth muscle to increase systemic blood pressure. Angiotensin II also acts on the adrenal cortex to release aldosterone, which increases renal Na+ reabsorption and K+ secretion.

FIGURE 9 Production of angiotensin II by the release of renin from juxtaglomerular cells. A variety of signals associated with falling blood pressure and/or extracellular fluid volume loss cause release of renin from juxtaglomerular cells. Renin acts as an enzyme to cleave angiotensin I from an a2-globulin, angiotensinogen. Angiotensin I is changed to angiotensin II by the cleavage of two amino acids, a process catalyzed by ACE. Angiotensin II acts on vascular smooth muscle to increase systemic blood pressure. Angiotensin II also acts on the adrenal cortex to release aldosterone, which increases renal Na+ reabsorption and K+ secretion.

reabsorption of Na+ as well as the secretion of K+ and protons. Thus, the release of renin has two actions that counteract any reduction of blood pressure and blood volume. Its pressor effects elevate the blood pressure, and its effects via aldosterone conserve Na+ and thus expand the extracellular fluid volume, which also indirectly elevates blood pressure and cardiac output (see also Chapter 29).

As might be expected if the RAS were involved in feedback regulation of blood pressure and volume, renin is released in response to signals that indicate a decrease in extracellular fluid volume, such as increased afferent sympathetic nerve input to the kidney. However, renin is also released in response to a fall in blood pressure that is sensed directly by the afferent arteriole. A fall in systemic blood pressure would cause renin release; however, a fall in the renal arterial pressure, independent of any change in systemic blood pressure, also causes renin release (see the Clinical Note on renovascular hypertension).

Renin-mediated hypertension may also be treated by drugs referred to as ACE inhibitors, which inhibit the formation of angiotensin II from its inactive precursor angiotensin I. The actions of angiotensin II can also be blocked by drugs that block its receptors. There are at least two angiotensin II receptors and the drugs now in common use block both. Investigators are currently working to identify differences in the actions of the two types of receptors, and type-specific receptor blockers have been developed, but it is presently unclear if there are advantages to blocking one or the other receptor type. Both ACE inhibitors and receptor antagonists have been extremely important antihypertensive drugs, especially in treating salt-sensitive hypertension with elevated plasma renin and hypertension in diabetic patients, who frequently develop kidney failure.

Because ACE is present in the kidney, renin secretion results in the production of angiotensin II in the renal cortex where it can act as a paracrine factor. Angioten-sin II increases proximal tubule volume absorption (see Chapter 26), and it acts directly on the afferent and efferent arterioles to increase their resistance, thus decreasing RBF and GFR. The RAS also responds to changes in salt delivery to the ascending limb of the loop of Henle and, thus, to the macula densa cells. In situations where the GFR is elevated or proximal tubule reabsorption of NaCl and water is diminished, for example, with isotonic volume expansion, there is an increased delivery of both to the loop of Henle. This results in an increased NaCl concentration at the end of the loop of Henle. The increased NaCl delivery is sensed by the macula densa cells, which signal adjacent juxtaglomerular cells to decrease renin secretion. A resulting decrease is seen in circulating angiotensin II levels and a corresponding decrease in aldosterone production, both of which would contribute to natri-uresis and diuresis.

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