Glossary of 7 - Prevention of spontaneous change in GFR

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What is the effective range of renal autoregulation?
Blood pressure of 80-180mmHg
How has it been proven that renal autoregulation is an intrinsic property?
This ability is maintained in kidneys that have been removed from the body.
At which part(s) of the kidney does renal autoregulation act?
At the smooth muscle of the afferent arterioles and interlobular arteries.
What is the "myogenic response"?
An increase in transmural pressure causes an increase in the conductance of Ca++ and release of endothelial factors - both of these cause vasoconstriction.
What function does the macula densa serve?
It senses the [NaCl] in the filtrate of the distal convoluted tubule; it can secrete NO, a vasodilator; signals granule cells and extraglomerular mesangial cells.
Other than renin, what mediators of vasoconstriction are released by the granular cells? Where are these cells located?
*ATP and adenosine
*they are specialized smooth muscle cells found in the wall of the afferent arterioles
What is a reason that renin is not likely to be involved in the short term autoregulation of blood flow to the glomeruli?
Release of renin in response to increased MAP will lead to an increase in angiotensin II. Angiotensin II preferentially constricts the efferent arteriole which would raise GFR and compound the problem, not rectify it.
What are the two main mechanisms of renal autoregulation?
1.Myogenic response
2.Tubuloglomerular feedback
What is the purpose of glomerulotubular balance?
It prevents large changes in water or salt excretion in the face of transient changes in GFR.
What is the theoretical basis for glomerulotubular balance?
The nephron reabsorbs a fractional quantity of filtered salt and water rather than an absolute amount.
How does an increase in GFR cause greater reabsorption of NaCl and water?
Increased GFR means more protein-free fluid is filtered out of the plasma, which increases the COP of the plasma in the peritubular capillaries...this leads to greater reabsorption, although, proportionally it is the same as that seen in normal GFR.
Under what conditions is the glomerulotubular balance (i.e. the fractional reabsorption) reset?
When ECV is greatly expanded or contracted, GT balance is reset to return ECV to normal. I.e. a new "fraction of reabsorption" is set.
How is GT balance "reset" when ECV is expanded?
Expansion of ECV results in greater hydrostatic pressure in the peritubular capillaries, thus less reabsorption takes place, effectively reducing the reabsoptive fraction.
What is the function of renal autoregulation?
It prevents changes in GFR due to transient changes in MAP.
How does tubuloglomerular feedback sense and respond to an increase in MAP?
Increased MAP is sensed as increased [NaCl] in the DCT by the macula densa. These cells signal the granular cells in the afferent arteriole which release vasoconstrictive substances such as ATP and adenosine. Constriction of the afferent arteriole lowers GFR back to an acceptable level.
How does tubuloglomerular feedback sense and respond to a decrease in MAP?
Decreased MAP is sensed as low [NaCl] in the DCT by the macula densa. These cells are able to release NO (a vasodilator) as well as signal the extraglomerular mesangial to release prostaglandins. Dilation of the afferent arteriole restores GFR to an acceptable level.
How does a decrease in GFR cause less reabsorption of NaCl?
A decrease in GFR results in the filtration of less protein-free fluid. This means that the COP in the peritubular capillaries is reduced, and reabsorption is no longer favored. Back leak increases, thus getting rid of excess fluid in the interstitium.

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