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 usuallythrough ETBreceptors.
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 effecton the kidney.
AVP caused a reduction in the lumen diameter of efferent arterioles, an
effect blocked by a specific V1receptor 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 A1receptors.

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.