One of the most basic and powerful mechanisms for the maintenance of sodium and fluid balance, as well as for controlling blood volume and extracellular fluid volume, is the effect of blood pressure on sodium and water excretion—called the pressure natriuresis and pressure diuresis mechanisms, respectively. As discussed in Chapter 19, this feedback also plays a dominant role in long-term blood pressure regulation.

Pressure diuresis refers to the effect of increased blood pressure to raise urinary volume excretion, whereas pressure natriuresis refers to the rise in sodium excretion that occurs with elevated blood pressure. Because pressure diuresis and natriuresis usually occur in parallel, we refer to these mechanisms simply as “pressure natriuresis” in the following discussion.

Figure 1 shows the effect of arterial pressure on urinary sodium output. Note that acute increases in blood pressure of 30 to 50 mm Hg cause a twofold to threefold increase in urinary sodium output. This effect is independent of changes in activity of the sympathetic nervous system or of various hormones, such as angiotensin II (Ang II), ADH, or aldosterone, because pressure natriuresis can be demonstrated in an isolated kidney that has been removed from the influence of these factors. With chronic increases in blood pressure, the effectiveness of pressure natriuresis is greatly enhanced because the increased blood pressure also, after a short time delay, suppresses renin release and, therefore, decreases formation of Ang II and aldosterone. As discussed previously, decreased levels of Ang II and aldosterone inhibit renal tubular reabsorption of sodium, thereby amplifying the direct effects of increased blood pressure to raise sodium and water excretion.

Fig1. Acute and chronic effects of arterial pressure on  sodium output by the kidneys (pressure natriuresis). Note that chronic  increases in arterial pressure cause much greater increases in sodium  output than those measured during acute increases in arterial  pressure. 

PRESSURE NATRIURESIS AND DIURESIS ARE KEY COMPONENTS OF A RENAL–BODY FLUID FEEDBACK FOR REGULATING BODY FLUID VOLUMES AND ARTERIAL PRESSURE

 The effect of increased blood pressure to raise urine output is part of a powerful feedback system that operates to maintain balance between fluid intake and output, as shown in Figure 2. This mechanism is the same mechanism that is discussed in Chapter 19 for arterial pressure control. The extracellular fluid volume, blood volume, cardiac output, arterial pressure, and urine output are all controlled at the same time as separate parts of this basic feedback mechanism.

Fig2. The basic renal–body fluid feedback mechanism for control of blood volume, extracellular fluid volume, and arterial pressure.  Solid lines indicate positive effects, and dashed lines indicate negative effects. 

During changes in sodium and fluid intake, this feedback mechanism helps to maintain fluid balance and to minimize changes in blood volume, extracellular fluid volume, and arterial pressure as follows:

1. An increase in fluid intake (assuming that sodium accompanies the fluid intake) above the level of urine output causes a temporary accumulation of fluid in the body.

 2. As long as fluid intake exceeds urine output, fluid accumulates in the blood and interstitial spaces, causing parallel increases in blood volume and extracellular fluid volume. As discussed later, the actual increases in these variables are usually small because of the effectiveness of this feedback.

3. An increase in blood volume raises mean circulatory filling pressure.

4. An increase in mean circulatory filling pressure raises the pressure gradient for venous return.

5. An increased pressure gradient for venous return elevates cardiac output.

6. An increased cardiac output raises arterial pressure.

7. An increased arterial pressure increases urine output by way of pressure diuresis. The steepness of the normal pressure natriuresis relation indicates that only a slight increase in blood pressure is required to raise urinary excretion severalfold.

 8. The increased fluid excretion balances the increased intake, and further accumulation of fluid is prevented.

Thus, the renal–body fluid feedback mechanism operates to prevent continuous accumulation of salt and water in the body during increased salt and water intake. As long as kidney function is normal and the pressure diuresis mechanism is operating effectively, large changes in salt and water intake can be accommodated with only slight changes in blood volume, extracellular fluid volume, cardiac output, and arterial pressure.

The opposite sequence of events occurs when fluid intake falls below normal. In this case, there is a tendency toward decreased blood volume and extracellular fluid volume, as well as reduced arterial pressure. Even a small decrease in blood pressure causes a large decrease in urine output, thereby allowing fluid balance to be maintained with minimal changes in blood pressure, blood volume, or extracellular fluid volume. The effectiveness of this mechanism in preventing large changes in blood volume is demonstrated in Figure 3, which shows that changes in blood volume are almost imperceptible despite large variations in daily intake of water and electrolytes, except when intake becomes so low that it is not sufficient to make up for fluid losses caused by evaporation or other inescapable losses.

Fig3. Approximate effect of changes in daily fluid intake on  blood volume. Note that blood volume remains relatively constant in  the normal range of daily fluid intakes. 

As discussed later, there are nervous and hormonal systems, in addition to intrarenal mechanisms, that can raise sodium excretion to match increased sodium intake even without measurable increases in cardiac output or arterial pressure in many persons. Other individuals who are more “salt sensitive” have significant increases in arterial pressure with even moderate increases in sodium intake. With prolonged high-sodium intake, lasting over several years, high blood pressure may occur even in persons who are not initially salt sensitive. When blood pressure does rise, pressure natriuresis provides a critical means of maintaining balance between sodium intake and urinary sodium excretion.

PRECISION OF BLOOD VOLUME AND EXTRACELLULAR FLUID VOLUME REGULATION

By studying Figure 2, one can see why the blood volume remains almost exactly constant despite extreme changes in daily fluid intake. The reason for this phenomenon is the following: (1) A slight change in blood volume causes a marked change in cardiac output, (2) a slight change in cardiac output causes a large change in blood pressure, and (3) a slight change in blood pressure causes a large change in urine output. These factors work together to provide effective feedback control of blood volume.

The same control mechanisms operate whenever there is a blood loss because of hemorrhage. In this case, a fall in blood pressure along with nervous and hormonal factors discussed later cause fluid retention by the kidneys. Other parallel processes occur to reconstitute the red blood cells and plasma proteins in the blood. If abnormalities of red blood cell volume remain, such as occurs when there is deficiency of erythropoietin or other factors needed to stimulate red blood cell production, the plasma volume will simply make up the difference, and the overall blood volume will return essentially to normal despite the low red blood cell mass.

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مواضيع ذات صلة

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

Multiple Functions of The Kidneys

التنظيم الحمضي – القاعدي في الجسم Acid-Base Balance

حصى الكلية Urinary Caliculi