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6 Pages

Kinesiology & Health Science
Course Code
KINE 2011
Gillian Wu

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21 March, 2012—Human physiology II What determines GFR? Two determinants (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 GFR is. 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 RESPONSE) 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 hydrostatic pressure. 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 circulation. 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 EFFERENT. 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 Vasoconstriction 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 overall GFR. Efferent vasoconstriction has an opposite effect on the glomerular filtration compared to afferent arteriole. *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
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