21 March, 2012—Human physiology II
What determines GFR?
(i) Kf (allow for fluid to pass through freely/ anatomical structures)
(ii) Net filtration pressure (summation of multiple forces how much fluid can move
through these anatomical openings available.
+ve pressure=Hydrostatic pressure within the Glomerulus.
-ve pressure= Hydrogstatic pressure within the Bowman space, generated by filterate.
--Osmotic pressure in the glomerular capillaries due to the plasma proteins that cannot
escape from the blood.
*The balance of these pressure will determine the GFR.
GFR can create big changes
Role of Hydrostatic Pressure
-Hydrostatic pressure within the glomerular capillaries is the dominant force
compared to other two pressures.
-Know the range of the numbers.
-Hydrostatic always creating forward pressure.
How GFR is affected by blood pressure?
-The hydrostatic pressure within the glomerulus is a key factor that determines what the
Anything that changes glomerular hydrostatic pressure will affect GFR.
If we increase arterial blood pressure by excercising or changing the posture, that
arterioal blood pressure is transmitted down the vascular tree, and we would see a
higher pressure as well within the glomerular capillaries (direct cause effect NOACTIVE
1 Increase arterial blood pressure = more flow going into the glomerulus, more blood will
fill the glomerulus, higher hydrostatic pressure forcing fluid out in to bowman space
causing higher GFR.
What is the impact of Vasoconstriction/Vasodilation of the AFFERENT ARTERIOLE?
Afferent arteriole & Efferent don’t have TO BE REGULATED SAME WAY in the KIDNEY
Vasoconstrict= decreases blood flow in the glomerulus; less fluid pressure within
glomerulus means that there will be less NET FILTERATION PRESSURE, since lower
So we generally reduce GFR.
Vasodilate=opening more flow to enter into glomerular; higher hydrostatic pressure will
further increase. Filtration rate will increase; more fluid will move from capillary into
bowman space and enter nephron structure.
The afferent arterioles are controlled by sympathetic nerves. The sympathetic nerves
will come down and terminate right beside afferent arterioles similar to systemic
Sympathetic nerves release norepinephrine which will bind to alpha adrenergic
receptors and cause vasoconstriction.(regulating vasoconstriction)
Active SNS there will be also epinephrine, if epinephrine is interacting with the afferent
arteriole. It will cause vasoconstriction. That’s because it will also bind to alpha
adrenergic receptors since there is NO BETA RECEPTORS.(unlike skeletal muscles)
-ANY SNS activity will cause vasoconstriction.
-Sympathetic nerves are more densely located in AFFERENT as compared to the
2 -Much stronger vasoconstriction at AFFERENT ARTERIOLES.
Vasodilation of the Afferent arterioles
-There are NO NERVES that will cause vasodilation.
-Nerves only STOP RELEASING Vasoconstrictor which causes Vasodilation.
Efferent can have same capacity to vasoconstrict and vasodilate.
Controlling the outflow from the glomerulus.
If we Vasoconstrict the efferent arteriole, how would it have an effect on the hydrostatic
pressure on the glomerulus?
It will increase, by restricting the outflow. That will increase filteration pressure and
Efferent vasoconstriction has an opposite effect on the glomerular filtration compared to
*THAT IS WHY EFFERENT AND AFFERENT ARTERIOLE SHOULD NOT BE
REGULATED THE SAME WAY*
Efferent don’t effect Afferent.
If Efferent Vasodilates, it allows more flow to exit the glomerulus, lower pressure in
glomerulus, filling pressure will drop and we will have reduction in GFR.
Afferent arterioles similar to systemic, but efferent have opposite influence since they
are down stream from the capillaries.
Changes in hydrostatic pressure within the glomerulus effect GFR.
3 -increase hydrostatic pres