The Physiology of the Afferent and
Efferent Arterioles
Role of the Afferent and Efferent
Arterioles
• The kidneys have an autoregulatory system to keep their
blood flow and perfusion constant over a wide range of
blood pressures.
• Unlike perfusion of all other organs, perfusion of the kidney
is not regulated to maintain organ nutrition but to retain its
filtration functions.
• The glomerular hydrostatic pressure is regulated mainly by
the balance of vascular tone in the afferent and efferent
arterioles.
• Owing to this exceptional arrangement of resistance vessels
in series, before and after the glomerulus, renal blood flow
(RBF) and glomerular filtration rate (GFR) can be regulated
independently.
• A selective increase in afferent resistance decreases RBF,
the blood flow into the glomerulus, and the glomerular
filtration pressure, a primary force for plasma
ultrafiltration.
• On the other hand, constriction of the efferent arteriole
raises glomerular filtration pressure, thereby maintaining or
even increasing GFR despite a drop in RBF and thus causing
an increase in filtration fraction (GFR/RBF).
• The vascular tone of these preglomerular and
postglomerular vessels is regulated by several systems,
including circulating hormones, paracrine factors, and the
renal sympathetic nerves.
Humoral Mechanisms Controlling
Afferent and Efferent Arteriolar
Resistance
• Angiotensin II
– A potent vasoconstrictor
– Causes a rise in filtration fraction
– Predominant action on the efferent arteriole
• Endothelin
– The endothelins are vasoconstrictor peptides mediated
usually through ETB receptors.
– Endothelin-1 (ET-1) causes renal vasoconstriction and a
decrease in RBF.
– The afferent arteriole is more sensitive to the
vasoconstrictor action of ET-1 than the efferent arteriole.
• Atrial Natriuretic Peptide
– Causes afferent arteriolar vasodilation and efferent arteriolar
vasoconstriction.
– The greater GFR resulted from a rise in glomerular pressure
– ANP has also been shown to reverse noradrenaline-induced afferent
vasoconstriction and to potentiate its efferent arteriolar
vasoconstriction.
– This action of ANP has been suggested to help maintain GFR in heart
failure,[28] in which ANP values are elevated and renal perfusion
pressure is reduced.
• Arginine Vasopressin
– Arginine vasopressin (AVP) is a potent vasoconstrictor, particularly in
the mesenteric circulation, with less effect on the kidney.
– AVP caused a reduction in the lumen diameter of efferent arterioles,
an effect blocked by a specific V1 receptor antagonist, but AVP had no
effect on afferent arterioles.
Paracrine Agents
• Nitric Oxide
– NO is a potent vasodilator.
– The afferent arteriole is more sensitive than the efferent arteriole to the
vasodilator effects of NO.
– The main action of NO is to modulate the action of angiotensin.
– L-NAME significantly augmented the vasoconstrictor action of angiotensin II in
afferent arterioles.
• Prostaglandins
– The major action of prostaglandins is to modulate the actions of
vasoconstrictors.
– The juxtamedullary afferent arteriolar response to angiotensin II is enhanced
by cyclooxygenase inhibition.
• Adenosine and ATP
– Adenosine evokes vasoconstriction.
– The vasoconstriction of afferent and efferent arterioles results from activation
of A1 receptors.
Control by the Sympathetic Nervous
System
• The kidney receives sympathetic innervation that
extends to the vascular smooth muscle cells,
juxtaglomerular renin-secreting cells, and mesangium
as well as the proximal and distal tubules and the loop
of Henle.
• The afferent arterioles are threefold more densely
innervated than the efferent arterioles.
• Differential innervation of the afferent and efferent
arterioles indicates that the sympathetic nervous
system evokes selective changes in preglomerular and
postglomerular resistance to regulate GFR and renal
function.
Effects of Drugs
• Calcium Antagonists
– Calcium antagonists cause preferential vasodilation of the afferent
arteriole.
– Action of a calcium antagonist may cause glomerular hypertension
that could lead to the progression of renal diseases.
• ACEI and AT-1 Antagonists
– Losartan and captopril increase RBF and GFR and decrease filtration
fraction through a reduction in total renal resistance due to a decrease
in efferent resistance.
• Dopamine
– Low-dose dopamine causes renal vasodilation.
– Dopamine produced dilation of the afferent arterioles and a smaller
degree of dilation of the efferent arterioles near the glomeruli.