renal hemodynamics 2 Flashcards
what is the relation between renal blood flow ( RBF ) and renal plasma flow ( RPF ) ?
go hand in hand and affect filtration
what is the difference between renal blood flow RBF and renal plasma flow RPF?
theres not much difference
but in filtration :
renal plasma flow is the portion of blood that is actually filtered so its important to distinguish while doing the calculation
what is the effect sympathetic nervous system on glomerular filtration ?
^^^Increase afferent resistance
increase efferent resistance
MAINLY AFFERENT CONSTRICTIONS
Lead to :
Decreased Glomerular filtration rate
+
^^^Decreased renal blood flow
Strong sympathetic nervous system activation —-> vasoconstriction of afferent and efferent arterioles —-> DECREASE GFR and RBF
Under normal condition —> Mild or moderate sympathetic stimulation of renal arterioles has LITTLE OR NO EFFECT ON GFR or RBF
In acute severe conditions —-> like SEVERE HEMORRHAGE —–> SEVERE INCREASE IN RESISTANCE DUE TO INCREASED SYMPATHETIC STIMULATIONS OF RENAL VESSELS —-> REDUCE GFR and RBF
what is the effect of catecholamines / norepinephrine on glomerular filtration rate?
similar to sympathetic
^^Increased resistance of AFFERENT arterioles
Increased resistance of EFFERENT arterioles
MAINLY AFFERENT CONSTRICTION
Lead to :
Decreased glomerular filtration
^^ DECREASED RENAL BLOOD FLOW
Norepinephrine and epinephrine released from adrenal medulla —> CONSTERTION OF AFFERENT AND EFFERENT ARTERIOLES —> decrease GFR and RBF decrease
They are like sympathetic , they only do a significant effect under crisis like hemorrhage but not under normal conditions
what is the angiotensin 2?
hormone activated in response to low blood pressure
hypovolemia via renin angiotensin system
what is the effect of angiotensin 2 on glomerular filtration rate?
selectively constrict efferent arterioles
Increase resistance of efferent arterioles
lead to :
initially increasing GFR , after prolonged activation lead to decrease GFR
Decrease renal blood flow ( cuz less blood is continued into the efferent arterioles )
NO EFFECT ON AFFERENT ARTERIOELS
preferably constricts the efferent arterioles in physiological conditions , POWERFULT RENAL VASOCONSTRICTION OF EFFERENT ARTEIOLES
why doesnt ang 2 work on afferent arterioles?
due to the release of nitric oxide and prostaglandins which will counteract the vasoconstrictions of ang 2
will escape by prostaglandin in paracrine fashion
what is the effect of prostaglandins on glomerular filtration rate?
Lead to vasodilation of efferent and afferent arterioles
MAINLY AFFERENT DILATION
^^^Decrease resistance of afferent arterioles ( blood flows faster )
Decreased resistance of efferent arterioles
lead to :
Increased GFR
^^ Increased RBF ( SIGNIFICANT )
Tend to increase GFR BUT IT IS NOT VERY IMPORTANT REGULATORS in normal conditions
IN stressful conditions such as after surgery or volume depletions, if the person is ON NSAIDS —> then prostaglandin synthesis may be decreased LEADING TO REDUCTION IN GFR —-> SO IT WONT LEAD TO VASODILATION AND AND INCREASE GFR and when lost it decreases GFR
IT IS IMPORTANT IN CRISIS BUT NOT UNDER NORMAL CONDITIONS
What is the effect of endothelin derived vasodilators ( NITRIC OXIDE ) on GFR?
Vasodilator of both :
^^^Decreased resistance of afferent arterioles
Decreased resistance of Efferent arterioles
MAINLY AFFERENT DILATIONS
Lead to :
Increased GFR
^^Increased RBF ( Significant (
MAINLY AFFERENT DILATION ( OPPOSE ANG 2 EFFECT ON AFFERENT ARTERIOLES )
Vasodilation of renal vessels and increased GFR , Basal level of NO is REQUIRED for vasodilation of kidneys , IN HYPERTENSIVE PATIENTS AND IN ATHEROSCLEROSIS CUZ OF DAMAGE TO ENDOTHELIUM —–> LESS NO is produced leads to increased RENAL VASOCONSTRICTIONS and elevation in BP
decrease GFR eventually and this is one of the mechanism of atherosclerosis leads to hypertension
what is the effect of endothelin on GFR?
VASOCONSTRCTIONS :
MAINLY AFFERENT CONSTRICTIONS
^^^Increased afferent resistance
Increased efferent resistance
leads to :
DECREASE GFR
^^Decreased RBF ( SIGINIFCANT )
Produced by damaged endothelial cells in conditions like chronic kidney disease and uremia , causing VASOCONSTRICTIONS and a reduction in BOTH GFR AND RBF
what does the kidney need to regulate?
kidneys need to regulate the GFR and renal blood flow, but of course , GFR more
if one is affected , the other is affected, so changes in blood pressure will affect both
what is autoregulation of GFR?
despite marked changes in BP, feedback mechanism inside the kidneys keep GFR at nearly constant
what is the significance of AUTOREGULATION OF GFR?
maintain a relatively constant GFR for the precise control of renal excretion of water and solutes
crucial for urine productions ensuring the body effectively eliminates waste and maintain water and electrolytes balance
each day approximately 180 liters of filtrate are produced without this process toxin substances would accumulate and fluid and electrolyte balance would be disrupted .
the kidneys have intrinsic regulations of auto regulation of GFR which is very tightly regulated kidneys need to regulate even with slight changes
How does autoregulation work on BP and GFR?
Bp drops —-> GFR decreases —> fluid retention
BP rise —-> GFR increase —> potentially dehydration
Mean arterial pressure range of 70-180 mmhg, kidneys is able to keep the GFR constant and allowing it to change by 10% up or down despite changes in BP
how is autoregulation achieved?
myogenic mechanism ( Smooth muscle response )
Macula densa feedback ( TUBULOGLOMERULAR FEEDBACK ) –> macula densa in juxtaglomerular apparatus sense sodium chloride levels and signals adjustments —> this communication between the tubular fluid in distal convoluted tubule and arterial blood in afferent and efferent nephrons
angiotensin 2
describe the myogenic mechanism ?
blood vessels can resist stretching
when BP increases
Vessels respond to increased wall tension by contraction of vascular smooth muscles
this contraction prevent excessive stretch of vessels wall and help prevent increase in RBF and GFR
intrinsic property of smooth muscles cells that helps regulate blood flow - when blood vessels are stretched beyond limit due to increased blood flow, the smooth muscle contracts automatically restrict the blood flow
Increased arterial pressure —->
Increased stretch of blood vessel —>
Increased Cell Calcium permeability —->
Increased intracellular calcium —->
Increased vascular resistance and contraction —->
The increased pressure will increase the flow
and then the increased resistance and contraction will reduce the blood flow counteract the increase
IF MAP is high then renal afferent arterioles constrict and resistance increase = RBF AND GFR flow remains constant Q = delta P/ R
Resistance is most important and significance
what are the 2 components of macula densa feedback mechanism?
tubuloglomerular feedback mechanism by macula densa has 2 components :
1— > afferent arteriolar feedback mechanism
2—-> efferent arteriolar feedback mechanism
what causes macula densa feedback mechansim?
special anatomical arrangement of JG apparatus when macula densa come in contact with AFFERENT AND EFFERENT ARTERIOLES
decrease in arterial blood pressure —–> less blood reaches the afferent arterioles ——> GFR decreases —-> RATE OF FLOW OF FLUID IN A LOOP OF HENLE DECREASE —-> MORE TIME TO INCREASE REABSORPTION OF SODIUM AND CHLORIDE
and by the time it reaches the Juxtaglomerular apparatus + distal convoluted tuble will sense REDUCED levels of NaCl by MACULA densa cells and WILL LEAD TOOO :
1- Afferent arteriolar vasodilation (less resistance )
2- angiotensin efferent arteriolar vasoconstriction ( more resistance )
increasing the GFR
both will help return of GFR towards normal
why does Efferent constrict ?
less sodium and chloride
macula densa signals the juxtaglomerular cells release renin activating RAAS system to raise to BP, where ANG 2 will constrict EFFERENT
is the afferent arteriole dilation part of myogenic mechanism?
it can be part of it
Myogenic mechanism is more potent when theres too much blood coming in , but this mechanism is more helpful when theres less blood flow and low blood pressure
describe the regulation of GFR by ang 2?
Decreased GFR —->
decreased macula densa NaCl —-?
Increased Renin release —->
Increased ANG 2 —->
Increased efferent arteriolar resistance —-?
increased blood pressure —>
Increase GFR
When bp and blood volume are low , macula densa sense low SODIUM CHLORIDE —> ang 2 level increases due to renin release —> increase efferent resistance —->
Causes the blood to pool in the glomerulus , this increases capillary hydrostatic pressure thereby raising the GFR
also due to efferent arteriolar constriction , blood flow in the peritubular capillaries decreases , giving more time for reabsorption of sodium chloride into the ECF, further contributing to the increase in blood volume and GFR
ang 2 is a potent vasoconstrictor of systemic vessels which help raise blood pressure
what are the effects of ang 2 ?
multiple effects :
stimulates ADH/vasopressin
promotes water reabsorption
trigger thrist
potent vasoconstrictor
release aldosterone
retain sodium and water
describe renal blood flow?
22-25% of cardiac output
1.2L/min
much in excess of metabolic demands of kidneys
90% of this CO is used by the kidneys in The cortex
1-2% of it is going to the medulla
why does the less blood goes to the medulla?
juxtamedullary nephrons do not need much blood
if it too much blood reaches the medulla , it could wash the essential solutes disrupting the necessary hyposomotic environent