Page 59 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Sodium and Water: Hypernatremia and Hyponatremia 49

despite spontaneous changes in GFR. This principle is Ingestion of a sodium load causes thirst, water con-
called glomerulotubular balance, and its mechanisms sumption, and expansion of ECF volume. These events
are incompletely understood. lead to a compensatory (secondary) increase in GFR
One mechanism is related to the fact that much of the by increasing hydrostatic pressure and decreasing oncotic
sodium in the proximal tubules is reabsorbed along with pressure in the glomerular capillaries. Increased stretching
several other solutes (e.g., glucose, amino acids, phos- of the afferent arterioles decreases renin secretion (and
phate, and bicarbonate). A spontaneous increase in GFR ultimately angiotensin II production). Volume expansion
increases the filtered load of all of these solutes, and their also causes increased atrial stretch, release of atrial
increased concentration in the proximal tubule enhances natriuretic peptide, and natriuresis.
sodium reabsorption. Changes in peritubular capillary There is a paradox here. How can an increase in GFR in
hydrostatic and oncotic pressures probably also play one situation cause an increase in the tubular reabsorption
an important role in glomerulotubular balance. If GFR of sodium and in another situation cause a decrease in
spontaneously increases without a change in renal plasma the tubular reabsorption of sodium? The answer to the
flow (RPF) (i.e., the filtration fraction increases), the paradox lies in the fundamental difference between
blood leaving the efferent arterioles has lower hydrostatic the kidneys’ reaction to a spontaneous (primary) increase
pressure and higher oncotic pressure, thus favoring water and their reaction to a compensatory (secondary) increase
and solute reabsorption in the proximal tubules (Fig. 3-3). in GFR. Glomerulotubular balance is evoked in the
Autoregulation (see Chapter 2) also contributes to former but not the latter situation.
glomerulotubular balance. When renal perfusion pressure
is increased, afferent arteriolar constriction prevents trans- Aldosterone
mission of the increased hydrostatic pressure to the glo- Changes in renal reabsorption of sodium in response to
merular capillaries and minimizes any increase in GFR dietary fluctuations in sodium intake are mediated by
and filtered solute load. the hormone aldosterone, which is synthesized in the
zona glomerulosa of the adrenal cortex. The production
and release of aldosterone are stimulated by angiotensin
Afferent arteriole Efferent arteriole
II, hyperkalemia, and adrenocorticotropic hormone
H 2 O Pr Na + H 2 O Pr Na +
(ACTH). Its release is inhibited by dopamine and atrial
natriuretic peptide. Aldosterone increases sodium reab-
sorption by increasing the number and activity of
open sodium channels in the luminal membranes of the
principal cells in the collecting ducts.
Peritubular capillary (Starling Forces)
Peritubular Capillary Factors

Bowman’s
H O Increased sodium intake leads to expansion of the ECF
space 2
Na + volume and compensatory increases in both GFR and
RPF (i.e., the filtration fraction remains unchanged).
This increases hydrostatic pressure and decreases oncotic
Renal tubule ↑ P T H O + ↓P cap sodium and water reabsorption in the proximal tubules.
pressure in the peritubular capillaries, thus reducing
2
Na
Decreased sodium intake leads to volume contraction.
↑π
↓ π
In this setting, RPF decreases more than GFR (i.e., the
cap
T
filtration fraction increases). This results in decreased
Figure 3-3 Effects of changes in Starling forces on tubular hydrostatic and increased oncotic pressures in the
reabsorption of water and sodium. If glomerular filtration rate peritubular capillaries and enhanced proximal tubular
(GFR) increases without a change in renal plasma flow (RPF) (or if
RPF decreases more than GFR as may occur in dehydration), the reabsorption of sodium and water (see Fig. 3-3).
filtration fraction (GFR/RPF) will increase (i.e., more water and Catecholamines
sodium will be filtered from the glomeruli into the Bowman space).
This sequence of events will result in lower hydrostatic pressure Catecholamine-induced vasoconstriction usually affects
(P cap ) and higher oncotic pressure (p cap ) in the peritubular capillaries the efferent more than the afferent arterioles. The resul-
(downstream from the glomerular capillaries) and higher tant increase in filtration fraction alters peritubular capil-
hydrostatic pressure (P T ) and lower oncotic pressure (p T ) in the lary hemodynamics so as to favor water and sodium
renal tubules (downstream from the Bowman space). These changes reabsorption (i.e., decreased hydrostatic pressure and
in Starling forces will facilitate water and sodium reabsorption from increased oncotic pressure). Catecholamines also directly
the tubular fluid into the peritubular capillaries, thus minimizing loss stimulate proximal tubular sodium reabsorption through
of water and sodium in the urine. (Drawing by Tim Vojt.)
an a 1 -adrenergic effect and stimulate renin release from