The synthesis and storage of atrial natriuretic peptide (ANP) by the myocytes of the cardiac atria is an additional mechanism that helps control renal NaCl excretion. ANP is released when the atria are distended and works to reduce blood pressure and increase the excretion of NaCl and water by the kidneys. Similarly, the ventricles of the heart produce brain natriuretic peptide (BNP), which is released when the ventricles are distended and has similar effects as ANP.

In the high-pressure arterial circuit, there are volume sensors called baroreceptors located in the aortic arch, carotid sinus, and afferent arterioles of the kidneys. These baroreceptors send signals to the brainstem through the glossopharyngeal and vagus nerves (cranial nerves IX and X). The response to this input influences sympathetic outflow and antidiuretic hormone (AVP) secretion. Decreased blood pressure leads to increased sympathetic nerve activity and AVP secretion, while increased pressure tends to reduce sympathetic nerve activity and activate parasympathetic nerve activity. The sensitivity of the high-pressure baroreceptors requires a 5% to 10% change in pressure to evoke a response.

The juxtaglomerular apparatus (JGA) in the kidneys, specifically the afferent arteriole, responds directly to changes in pressure. When the perfusion pressure in the afferent arteriole decreases, it triggers the release of renin from the granular cells. Conversely, renin secretion is suppressed when perfusion pressure increases. Renin plays a role in determining the levels of angiotensin II and aldosterone in the blood, both of which reduce renal NaCl excretion.

If a renal artery is constricted, such as by an atherosclerotic plaque, the perfusion pressure to that kidney decreases. This reduction in perfusion pressure is sensed by the afferent arteriole of the JGA, resulting in renin secretion. The elevated renin levels increase the production of angiotensin II, which raises systemic blood pressure by constricting arterioles throughout the vascular system. The increased systemic blood pressure is sensed by the JGA of the contralateral kidney (the kidney without stenosis of its renal artery), leading to the suppression of renin secretion from that kidney. Additionally, the high levels of angiotensin II also inhibit renin secretion by the contralateral kidney through negative feedback. Treatment options for patients with constricted renal arteries include surgical repair of the stenotic artery, administration of angiotensin II receptor blockers, or administration of an angiotensin-converting enzyme (ACE) inhibitor, which blocks the conversion of angiotensin I to angiotensin II.

When the volume sensors in the vascular system detect a change in extracellular fluid volume (ECFV), they send signals to the kidneys, resulting in an appropriate adjustment in NaCl and water excretion. If the ECFV expands, renal NaCl and water excretion increase. Conversely, if the ECFV contracts, renal NaCl and water excretion decrease. The signals involved in connecting the volume sensors to the kidneys are both neural and hormonal. These effects and mechanisms are summarized in Box 35.1.
The cardiac atria possess an additional mechanism related to control of renal NaCl excretion. The myocytes of the atria synthesize and store a peptide hormone, atrial natriuretic peptide (ANP). It is released when the atria are distended and, via mechanisms outlined later in this chapter, reduces blood pressure and increases excretion of NaCl and water by the kidneys. The ventricles of the heart also produce a natriuretic peptide, brain natriuretic peptide (BNP), so named because it was first isolated from the brain. Like ANP, BNP is released from myocytes by distention of the ventricles. Its actions are similar to those of ANP.
Volume Sensors in the High-Pressure Arterial Circuit
Baroreceptors are also present in the arterial side of the circulatory system, located in the wall of the aortic arch, carotid sinus, and afferent arterioles of the kidneys. The aortic arch and carotid baroreceptors send input to the brainstem via afferent fibers in the glossopharyngeal and vagus nerves (cranial nerves IX and X). The response to this input alters sympathetic outflow and AVP secretion. Thus a decrease in blood pressure increases sympathetic nerve activity and AVP secretion. An increase in pressure tends to reduce sympathetic nerve activity (and activate parasympathetic nerve activity). The sensitivity of the high-pressure baroreceptors is similar to that in the low-pressure side of the vascular system; 5% to 10% changes in pressure are needed to evoke a response.
The juxtaglomerular apparatus (JGA) of the kidneys (see ), particularly the afferent arteriole, responds fThe liver and central nervous system also have sensors that respond to changes in blood pressure and [Na+] and then signal the kidneys to alter NaCl excretion. These systems do not appear to be as important as vascular receptors in monitoring changes in ECFV and effecting changes in renal NaCl excretion and are not considered here.
directly to changes in pressure. If perfusion pressure in the afferent arteriole is reduced, renin is released from the granular cells. By contrast, renin secretion is suppressed when perfusion pressure is increased. As described later in this chapter, renin determines blood levels of angiotensin II and aldosterone, both of which reduce renal NaCl excretion.
Constriction of a renal artery (e.g., by an atherosclerotic plaque) reduces perfusion pressure to that kidney. This reduced perfusion pressure is sensed by the afferent arteriole of the JGA and results in renin secretion. The elevated renin levels increase the production of angiotensin II, which in turn increases systemic blood pressure via its vasoconstrictor affect on arterioles throughout the vascular system. The increased systemic blood pressure is sensed by the JGA of the contralateral kidney (i.e., the kidney without stenosis of its renal artery), and renin secretion from that kidney is suppressed. In addition the high levels of angiotensin II also inhibit renin secretion by the contralateral kidney (negative feedback). Treatment of patients with constricted renal arteries includes surgical repair of the stenotic artery, administration of angiotensin II receptor blockers, or administration of an inhibitor of angiotensin-converting enzyme (ACE). The ACE inhibitor blocks conversion of angiotensin I to angiotensin II.
When the vascular volume sensors have detected a change in ECFV, they send signals to the kidneys, which results in an appropriate adjustment in NaCl and water excretion. Accordingly, when the ECFV is expanded, renal NaCl and water excretion are increased. Conversely, when the ECFV is contracted, renal NaCl and water excretion are reduced. The signals involved in coupling the volume sensors to the kidneys are both neural and hormonal. These are summarized in
Box 35.1 , as are their effects on renal NaCl and water excretion.