Page 40 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Applied Renal Physiology 29

60 60 Afferent Efferent
Control
50 Net ultrafiltration 50
pressure 40
Pressure (mm Hg) 30 π GC P GC 30 Decreased = ↑RBF ↑GFR
40
resistance
in afferent

20
20
Increased
10 P T 10 resistance = ↓RBF ↓GFR
in afferent

0 Distance along glomerular capillary 100%
(Afferent end) (Efferent end)
Decreased
resistance ↑RBF ↓GFR
Mean values for dog and cat in efferent
P GC Hydrostatic pressure in glomerular capillary 52 58
π GC Plasma oncotic pressure in glomerular capillary 20 22
Hydrostatic pressure in Bowman’s space 20 18
P T Increased
π T Oncotic pressure in Bowman’s space 0 0 resistance = ↓RBF ↑GFR
in efferent
Net ultrafiltration pressure 12 18
Figure 2-4 Graphic representation of the generation of net
filtration pressure in the glomerulus as governed by Starling
forces. (Drawing by Tim Vojt.) Figure 2-5 Effects of alterations in afferent and efferent arteriolar
tone on renal blood flow and glomerular filtration rate. (Drawing by
Tim Vojt.)
systemic capillaries accounts for the much higher rate of
filtration. The ultrafiltration coefficient, K f , is not con- afferent and efferent vasodilatation and increased RBF
stant and can change as a result of disease and in response with little change in GFR at low concentrations of dopa-
to hormones that cause mesangial cells to contract (e.g., mine. Norepinephrine, angiotensin II, and antidiuretic
angiotensin II). hormone (ADH, vasopressin) cause vasoconstriction, at
Changes in the resistance of the afferent the same time promoting the production of prosta-
(preglomerular) and efferent (postglomerular) arterioles glandins that cause vasodilatation. These prostaglandins
may have a marked effect on GFR. Alterations in resis- (PGE 2 and PGI 2 ) play an important role in maintaining
tance in the afferent arterioles lead to parallel changes RBF in hypovolemic states when angiotensin II and nor-
in GFR and renal blood flow (RBF), but changes in resis- epinephrine concentrations are increased. The effects of
tance in the efferent arterioles lead to divergent changes these prostaglandins are limited to the kidneys because
in GFR and RBF (Fig. 2-5). The interplay of the effects of they are rapidly metabolized in the pulmonary circula-
neural and hormonal factors on vascular tone in the tion. Nonsteroidal anti-inflammatory drugs that inhibit
kidneys is complex, but the main purpose of these effects generation of prostaglandins by the cyclooxygenase path-
is to minimize even slight changes in GFR, which could way may cause renal ischemia and acute renal insufficiency
have drastic adverse effects on the volume and composi- in hypovolemic patients. 10,12 Locally produced kinins
tion of the extracellular fluid. also cause vasodilatation and favor redistribution of
The resistance of these arterioles is regulated by the RBF to inner cortical nephrons. Mediators produced
autonomic nervous system and by numerous vasoactive locally by the vascular endothelium also contribute to
mediators (Table 2-1). Stimulation of the sympathetic afferent and efferent vasoconstriction (e.g., endothelin
nervous system results in release of norepinephrine from and thromboxane) and vasodilatation (e.g., nitric oxide
nerves terminating on the afferent and efferent arterioles. and prostacyclin).
Norepinephrine can cause afferent and efferent vasocon-
striction, but efferent arteriolar constriction usually MEASUREMENT OF GLOMERULAR
predominates. As a result, RBF decreases with minimal FILTRATION RATE
changes in GFR (i.e., filtration fraction [FF] increases). Consider a substance that is filtered by the glomeruli but
Angiotensin II also causes efferent more than afferent neither reabsorbed nor secreted by the tubules. Under
vasoconstriction and has similar effects on RBF and steady-state conditions, the following mass balance
GFR. Stimulation of dopaminergic receptors causes equation may be written: