Sensing Of Extracellular Fluid Volume

The large veins and atria possess receptors that sense relative vascular filling and, thus, plasma volume. These receptors are neural stretch receptors that increase their rate of firing as the wall of the vessel is expanded in much the same way as the stretch receptors of the carotid sinus (see Chapter 15). The venous stretch receptors are probably the volume receptors that modulate vasopressin release from the posterior pituitary and that can override the normal signals of plasma osmolality in regulating vasopressin release. As discussed later, the atria can also release a peptide (atrial natriuretic peptide) that may regulate renal Na+ excretion directly.

Distension of the large veins in the thorax or distension of the atria results in a relatively rapid response of natriuresis and diuresis. Arterial barorecep-tors also seem to be important in regulating this response. It is likely that there are arterial stretch receptors similar to those located in the carotid sinus that respond to an increase in arterial blood pressure or pulse pressure with an increase in firing. With decreased stretch of these receptors, which would occur with a falling cardiac output or a diminished plasma volume, the renal excretion of Na+ and water falls rapidly. The afferent neural arcs that carry the information from stretch receptors in the atria and large veins run primarily with parasympathetic fibers in the vagus nerve. These fibers impinge on the central nervous system in a variety of different centers that may be associated with the regulation of vasopressin secretion, sympathetic firing to the kidneys, and cardiovascular centers among others.

What factors normally stimulate these volume receptors? First, an actual decrease in extracellular volume due to dehydration leads to a decrease in plasma volume with a fall in central venous pressure and atrial filling by venous return. This decreases stretch in the walls of both the venous and arterial volume receptors, eventually leading to an appropriate retention of Na+. Second, there could be a decrease in plasma volume with a normal or increased ECF volume (see Clinical Note on edema earlier in this chapter). The decreases in venous and arterial filling lead to retention of Na+ by the kidneys. Finally, under conditions of normal or expanded ECF volume when cardiac output is decreased or effective perfusion of the tissues is decreased because of heart failure, there is a strong stimulus for Na+ retention despite the expanded ECF volume. Thus, for example, heart failure is often accompanied by extracellular volume expansion, resulting in a progression from peripheral edema to pulmonary edema and eventual decompensation of cardiac contraction due to excessive ventricular filling. This general condition is referred to as functional hypovolemia (see following Clinical Note)—the body is reacting to the poor tissue perfusion as if it were due to a low circulating blood volume, whereas the blood volume may, in fact, be dangerously expanded.

In the remainder of the chapter, the emphasis is on how these signals indicating a change in ECF volume result in changes in the rate of Na+ excretion by the kidney. This is obviously one of the most important functions of the kidney, and it is vital to the maintenance of normal cardiac output and blood pressure and, thus, to survival. Multiple mechanisms regulate Na+ reabsorption in various segments of the nephron, but the apparent redundancy of these mechanisms may have a survival advantage in that the failure of one will not lead to catastrophe. Nevertheless, it is clear that a better understanding of the interrelation among the various mechanisms must be achieved before we can fully understand the regulation of Na+ excretion under normal physiologic circumstances, as well as in pathologic derangements that lead to such conditions as hypertension and congestive heart failure.


The regulation of Na+ excretion by the kidney is accomplished by three basic mechanisms, each of which is also influenced by other signaling systems. In general, a reduction in GFR is associated with Na+ retention, and an increase in GFR enhances Na+ excretion. The second mechanism, aldosterone, controls Na+ reabsorption in the CNT and principal cells of the connecting tubule and the collecting duct, i.e., the aldosterone-responsive distal nephron (ARDN). The third mechanism also depends primarily on changing the rate of Na+ reabsorption by the nephron through the effects of natriuretic hormones on transport.

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