Sensors of Volume
Baroreceptors are the principal volume receptors in the body. Because blood pressure is the product of cardiac output and systemic vascular resistance, significant changes in intravascular volume (preload) not only affect cardiac output but also transiently affect arterial blood pressure. Thus, the baroreceptors at the carotid sinus and afferent renal arterioles (juxtaglomerular apparatus) indirectly function as sensors of intravascular volume. Changes in blood pressure at the carotid sinus modulate sympathetic nervous system activity and nonosmotic ADH secretion, whereas changes at the afferent renal arterioles modulate the renin-angiotensin-aldosterone system. Stretch receptors in both atria are affected by changes in intravascular volume, and the degree of atrial distention modulates the release of atrial natriuretic hormone and ADH.
Regardless of the mechanism, effectors of volume change ultimately alter urinary Na+ excretion. Decreases in “effective” intravascular volume decrease urinary Na+ excretion, whereas increases in the “effective” intravascular volume increase urinary Na+ excretion. These mechanisms include the following:Effectors of Volume Change
Renin secretion increases the formation of angiotensin II. The latter increases the secretion of aldosterone and has a direct effect in enhancing Na+ reabsorption in the proximal renal tubules. Angiotensin II is also a potent direct vasoconstrictor and potentiates the actions of norepinephrine. Secretion of aldosterone enhances Na+ reabsorption in the distal nephron (see Chapter 29) and is a major determinant of urinary Na+ excretion.
This peptide is normally released from both right and left atrial cells following atrial distention. ANP appears to have two major actions: arterial vasodilation and increased urinary sodium and water excretion in the renal collecting tubules. Na+-mediated afferent arteriolar dilation and efferent arteriolar constriction can also increase glomerular filtration rate (GFR). Other effects include the inhibition of both renin and aldosterone secretion and antagonism of ADH.
ANP, BNP, and C-type natriuretic peptide are structurally related peptides. BNP is released by the ventricles in response to increased ventricular volume and pressure, and ventricular overdistention, and also by the brain in response to increased blood pressure. BNP levels are usually approximately 20% of ANP levels, but during an episode of acute congestive heart failure BNP levels may exceed those of ANP. BNP levels can be measured clinically, and a recombinant form of BNP, nesiritide (Natrecor), is available to treat acute decompensated congestive heart failure.
Enhanced sympathetic activity increases Na+ reabsorption in the proximal renal tubules, resulting in Na+ retention, and increases renal vasoconstriction, which reduces renal blood flow (see Chapter 29). Conversely, stimulation of left atrial stretch receptors results in decreases in renal sympathetic tone and increases in renal blood flow (cardiorenal reflex) and glomerular filtration.
The amount of Na+ filtered in the kidneys is directly proportionate to the product of the GFR and plasma Na+ concentration. Because GFR is usually proportionate to intravascular volume, intravascular volume expansion can increase Na+ excretion. Conversely, intravascular volume depletion decreases Na+ excretion. Similarly, even small elevations of blood pressure can result in a relatively large increase in urinary Na+excretion because of the resultant increase in renal blood flow and glomerular filtration rate. Blood pressure-induced diuresis (pressure natriuresis) appears to be independent of any known humorally or neurally mediated mechanism.
Despite wide variations in the amount of Na+ filtered in nephrons, Na+reabsorption in the proximal renal tubules is normally controlled within narrow limits. Factors considered to be responsible for tubuloglomerular balance include the rate of renal tubular flow and changes in peritubular capillary hydrostatic and oncotic pressures. Altered Na+ reabsorption in the proximal tubules can have a marked effect on renal Na+ excretion.
Although ADH secretion has little effect on Na+ excretion, nonosmotic secretion of this hormone (see above) can play an important part in maintaining extracellular volume with moderate to severe decreases in the “effective” intravascular volume.
In summary, the multiple mechanisms involved in regulating ECF volume and sodium balance normally complement one another but can function independently. In addition to altering renal Na+ excretion, some mechanisms also produce more rapid compensatory hemodynamic responses when “effective” intravascular volume is reduced.
Extracellular fluid volume regulation generally takes precedence over osmoregulation.