One of the body’s most powerful controllers of sodium excretion is Ang II. Changes in sodium and fluid intake are associated with reciprocal changes in Ang II formation, and this in turn contributes greatly to the maintenance of body sodium and fluid balances. That is, when sodium intake is elevated above normal, renin secretion is decreased, causing decreased Ang II formation. Because Ang II has several important effects to increase tubular reabsorption of sodium, as explained in Chapter 28, a reduced level of Ang II decreases tubular reabsorption of sodium and water, thus increasing the kidneys’ excretion of sodium and water. The net result is to minimize the rise in extracellular fluid volume and arterial pressure that would otherwise occur when sodium intake increases.

Conversely, when sodium intake is reduced below normal, increased levels of Ang II cause sodium and water retention and oppose reductions in arterial blood pressure that would otherwise occur. Thus, changes in activity of the renin-angiotensin system act as a powerful amplifier of the pressure natriuresis mechanism for maintaining stable blood pressures and body fluid volumes.

Importance of Changes in Ang II in Altering Pressure Natriuresis. The importance of Ang II in making the pressure natriuresis mechanism more effective is shown in Figure 1. Note that when the angiotensin control of natriuresis is fully functional, the pressure natriuresis curve is steep (normal curve), indicating that only minor changes in blood pressure are necessary to increase sodium excretion when sodium intake is raised.

Fig1. Effects of excessive angiotensin II (Ang II) formation  or blocking Ang II formation on the renalpressure natriuresis curve.  Note that high levels of Ang II formation decrease the slope of pressure natriuresis, making blood pressure very sensitive to changes in  sodium intake. Blockade of Ang II formation shifts pressure natriuresis to lower blood pressures. 

In contrast, when angiotensin levels cannot be decreased in response to increased sodium intake (high angiotensin II curve), as occurs in some hypertensive patients who have impaired ability to decrease renin secretion and Ang II formation, the pressure natriuresis curve is not nearly as steep. Therefore, when sodium intake is raised, much greater increases in arterial pressure are necessary to increase sodium excretion and maintain sodium balance. For example, in most people, a 10-fold increase in sodium intake causes an increase of only a few millimeters of mercury in arterial pressure, whereas in subjects who cannot suppress Ang II formation appropriately in response to excess sodium, the same rise in sodium intake causes blood pressure to rise as much as 50 mm Hg. Thus, the inability to suppress Ang II formation when there is excess sodium reduces the slope of pressure natriuresis and makes arterial pressure very salt sensitive, as discussed in Chapter 19.

The use of drugs to block the effects of Ang II has proved to be important clinically for improving the kidneys’ ability to excrete salt and water. When Ang II formation is blocked with an angiotensin-converting enzyme inhibitor (see Figure 30-17) or an Ang II receptor antagonist, the renal-pressure natriuresis curve is shifted to lower pressures, which indicates an enhanced ability of the kidneys to excrete sodium because normal levels of sodium excretion can now be maintained at reduced arterial pressures. This shift of pressure natriuresis provides the basis for the chronic blood pressure lowering effects of the angiotensin-converting enzyme inhibitors and Ang II receptor antagonists in hypertensive patients.

Excessive Ang II Does Not Usually Cause Large Increases in Extracellular Fluid Volume Because Increased Arterial Pressure Counterbalances Ang II–Mediated Sodium Retention. Although Ang II is one of the most powerful sodium- and water-retaining hormones in the body, neither a decrease nor an increase in circulating Ang II has a large effect on extracellular fluid volume or blood volume as long as heart failure or kidney failure does not occur. The reason for this phenomenon is that with large increases in Ang II levels, as occurs with a renin-secreting tumor of the kidney, the high Ang II levels initially cause sodium and water retention by the kidneys and a small increase in extracellular fluid volume. This also initiates a rise in arterial pressure that quickly increases kidney output of sodium and water, thereby overcoming the sodium- and water-retaining effects of the Ang II and re-establishing a balance between intake and output of sodium at a higher blood pressure. Conversely, after blockade of Ang II formation, as occurs when an angiotensin-converting enzyme inhibitor is administered, there is initial loss of sodium and water, but the fall in blood pressure rapidly offsets this effect and sodium excretion is once again restored to normal.

If the heart is weakened or there is underlying heart disease, cardiac pumping ability may not be great enough to raise arterial pressure enough to overcome the sodium retaining effects of high levels of Ang II; in these instances, Ang II may cause large amounts of sodium and water retention that may progress to congestive heart failure. Blockade of Ang II formation may, in these cases, relieve some of the sodium and water retention and attenuate the large expansion of extracellular fluid volume associated with heart failure.

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مواضيع ذات صلة

Role of Aldosterone in Controlling Renal Excretion

Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes

Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance

Integration of Renal Mechanisms for Control of Extracellular Fluid

Osmoreceptor-ADH Feedback System

Urine Specific Gravity

Renal Mechanisms for Excreting Dilute Urine

Physiological Control of Glomerular Filtration and Renal Blood Flow

Renal Blood Flow

Determinants of The GFR

Glomerular Filtration—The First Step in Urine Formation

Urine Formation Results From Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion