Ganong's Review of Medical Physiology, 23rd Edition

644 SECTION VIII Renal Physiology
From the renal plasma flow, the renal blood flow can be calculated
by dividing by 1 minus the hematocrit:
Hematocrit (Hct): 45%
Renal blood flow = RPF × 1
1–Hct
= 700 × 1
0.55
= 1273 mL/min
PRESSURE IN RENAL VESSELS
The pressure in the glomerular capillaries has been measured
directly in rats and has been found to be considerably lower
than predicted on the basis of indirect measurements. When the
mean systemic arterial pressure is 100 mm Hg, the glomerular
capillary pressure is about 45 mm Hg. The pressure drop across
the glomerulus is only 1 to 3 mm Hg, but a further drop occurs
in the efferent arteriole so that the pressure in the peritubular
capillaries is about 8 mm Hg. The pressure in the renal vein is
about 4 mm Hg. Pressure gradients are similar in squirrel monkeys
and presumably in humans, with a glomerular capillary
pressure that is about 40% of systemic arterial pressure.
REGULATION OF THE
RENAL BLOOD FLOW
Norepinephrine (noradrenaline) constricts the renal vessels,
with the greatest effect of injected norepinephrine being exerted
on the interlobular arteries and the afferent arterioles. Dopamine
is made in the kidney and causes renal vasodilation
and natriuresis. Angiotensin II exerts a constrictor effect on
both the afferent and efferent arterioles. Prostaglandins increase
blood flow in the renal cortex and decrease blood flow
in the renal medulla. Acetylcholine also produces renal vasodilation.
A high-protein diet raises glomerular capillary pressure
and increases renal blood flow.
FUNCTIONS OF THE RENAL NERVES
Stimulation of the renal nerves increases renin secretion by a
direct action of released norepinephrine on β 1-adrenergic receptors
on the juxtaglomerular cells (see Chapter 39) and it increases
Na + reabsorption, probably by a direct action of
norepinephrine on renal tubular cells. The proximal and distal
tubules and the thick ascending limb of the loop of Henle are
richly innervated. When the renal nerves are stimulated to increasing
extents in experimental animals, the first response is
an increase in the sensitivity of the juxtaglomerular cells
(Table 38–2), followed by increased renin secretion, then increased
Na + reabsorption, and finally, at the highest threshold,
renal vasoconstriction with decreased glomerular filtration
and renal blood flow. It is still unsettled whether the effect on
TABLE 38–2 Renal responses to graded renal nerve
stimulation.
Renal
Nerve
Stimulation
Frequency
(Hz) RSR a
0.25 No effect on basal values;
augments RSR mediated
by nonneural stimuli.
0.50 Increased without changing
U NAV, GFR, or RBF.
1.0 Increased with decreased
without changing GFR or
RBF.
2.50 Increased with decreased
U NAV, GFR, and RBF.
Na + reabsorption is mediated via α- or β-adrenergic receptors,
and it may be mediated by both. The physiologic role of
the renal nerves in Na + metabolism is also unsettled, in part
because most renal functions appear to be normal in patients
with transplanted kidneys, and it takes some time for transplanted
kidneys to acquire a functional innervation.
Strong stimulation of the sympathetic noradrenergic nerves
to the kidneys causes a marked decrease in renal blood flow.
This effect is mediated by α 1 -adrenergic receptors and to a lesser
extent by postsynaptic α 2 -adrenergic receptors. Some tonic discharge
takes place in the renal nerves at rest in animals and
humans. When systemic blood pressure falls, the vasoconstrictor
response produced by decreased discharge in the baroreceptor
nerves includes renal vasoconstriction. Renal blood flow is
decreased during exercise and, to a lesser extent, on rising from
the supine position.
AUTOREGULATION OF
RENAL BLOOD FLOW
U NAV GFR RBF a
0 0 0
0 0 0
↓ 0 0
↓ ↓ ↓
aRSR, renin secretion rate; , urinary sodium excretion; RBF, renal blood flow.
Reproduced from DiBona GF: Neural control of renal function: Cardiovascular implications.
Hypertension 1989;13:539. By permission of the American Heart Association.
When the kidney is perfused at moderate pressures (90–220
mm Hg in the dog), the renal vascular resistance varies with
the pressure so that renal blood flow is relatively constant
(Figure 38–4). Autoregulation of this type occurs in other organs,
and several factors contribute to it (see Chapter 33). Renal
autoregulation is present in denervated and in isolated,
perfused kidneys, but is prevented by the administration of
drugs that paralyze vascular smooth muscle. It is probably
produced in part by a direct contractile response to stretch of
the smooth muscle of the afferent arteriole. NO may also be
involved. At low perfusion pressures, angiotensin II also appears
to play a role by constricting the efferent arterioles, thus