test 7 part 2 Flashcards
(30 cards)
RBF and Oxygen Consumption
RBF provides flow for basic metabolic needs of kidneys and excess flow for plasma filtration
Renal O2 consumption is 2x that of the brain BUT renal blood flow is 7x greater
Most of O2 consumed supports sodium reabsorption – consumption directly related to rate of sodium reabsorption
-O2 consumption in the kidney depends on how much Na we are reabsorbing
-as Na reabsorption goes up => O2 consumption goies up
-Na/K pumps are what cause an increase in O2 consumption
Determinants of RBF
(Renal artery pressure – Renal vein pressure) / Total renal resistance
Arterial ≈ 100 mmHg; Venous ≈ 4 mmHg
Percentage of renal vascular resistance
Afferent arterial ≈ 26%
Efferent arterial ≈ 43% (more constricted than afferent arterial)
Interlobar, arcuate, interlobular arteries ≈ 16%
Account for 85% total renal resistance
Resistance of these three areas controlled by sympathetic nervous system, hormones, local control within kidneys
Flow Distribution Within Kidney
98 to 99% of flow goes to renal cortex (majority of the nephrons)
1 to 2% of flow goes to renal medulla via the vasa recta
Key part of ability to concentrate urine
Effect of Sympathetic Activation
All vessels receive sympathetic innervation
Strong activation – Constriction
Decrease RBF and GFR
Mild to moderate activation (moderate decrease in BP with corresponding baroreceptor response)
Little effect on RBF or GFR
Most important when body faced with life threatening problem
Severe hemorrhage
Healthy normal person – very little effect
Hormonal Effect of Epi, Norepi, Endothelin
Epinephrine and norepinephrine
Effect similar to effect of sympathetic nervous system
Endothelin
Released by damaged vascular endothelial cells of kidneys and other tissue – play role in hemostasis??
Concentration increased during toxemia of pregnancy, acute renal failure, chronic uremia
Powerful vasoconstrictor
Hormonal Effect of Angiotensin II
Potent vasoconstrictor that is normally circulating and is produced locally
All renal vessels contain receptors but preglomerular vessels show weak if any response because of simultaneous release of vasodilators such as nitric oxide and prostaglandins
Strong effect on efferent arterial producing increased glomerular
pressure AND decreased renal blood flow
Helps reduce decrease in GFR during times of decreased MAP and/or volume depletion
Enhanced tubular reabsorption because of decreased flow thru peritubular capillaries
Hormonal Effect of Nitric Oxide
Renal endothelial cells release a basal level that
helps maintain dilation of renal vessels
Giving nitric oxide inhibitor
Increases renal vascular resistance
Decreases GFR & urinary excretion of sodium
If continued will result in an increase in MAP due to the increased sodium levels
Hormonal Effect of Bradykinin & Prostaglandins
Potent vasodilators
Tend to increase RBF and GFR
Do not appear to have major impact during normal conditions
May dampen effect of sympathetic nerves and angiotensin II
May help prevent excessive decreases in RBF and GFR
Inhibited by administration of nonsteroidal anti-inflammatory agents
Autoregulation of RBF & GFR
Mechanisms are intrinsic to the kidneys
Function without systemic or neural influence
Purpose is to maintain NORMAL GFR and allow control of renal excretion of water and solutes
Prevents big changes in water / solute excretion with normal changes in blood pressure
Decreasing MAP to 75 mmHg or increasing to 160 mmHg results in a small change in GFR (<10% change)
RBF not as well controlled as GFR
What Would Happen If No Autoregulation
Increased MAP 100 to 125 mmHg
GFR would go from 180 L/day to 225 L/day
If reabsorption then remained constant:
225 – 178.5 = 46.5 L/day of urine output
Would quickly deplete the circulating blood volume
Large increase in urine output prevented by
Autoregulation
Changes in tubular reabsorption
But urine output and solute excretion DOES increase with an increase in MAP
The big changes in urine output
- changes in autoregulation
- changes in tubular reabsorption
- as GFR goes up you see an increase in reabsorption (don’t go up at the same rate)
Tubuloglomerular Feedback Mechanism
Links autoregulation of GFR and RBF to the amount of NaCl entering the distal tubule
Regulates RBF and GFR in parallel
GFR regulation rather than RBF regulation plays larger role in maintaining constant delivery of NaCl to distal tubule
Components
Afferent arteriole feedback mechanism
Efferent arteriole feedback mechanism
Juxtaglomerular complex
Juxtaglomerular Complex - macula densa cells
Macula densa cells
Epithelial cells located initial part of distal tubule
In contact with portions of afferent & efferent arterioles
Contain secretory Golgi apparatus
Sense changes in NaCl concentration in the tubular fluid
Juxtaglomerular Complex - Juxtaglomerular cells
Surround afferent arteriole where it enters the glomerulus
Surround efferent arteriole where it leaves glomerulus
In contact with portion of distal tubule that contains macula densa
PRODUCE RENIN
Juxtaglomerular Complex - Operation
Believed that macula densa monitors amount of volume delivered to distal tubule via NaCl concentration
As GFR decreases
Flow rate through Loop Henle also decreases
Reabsorption of Na+ and Cl- in loop increases
Concentration Na+ and Cl- at macula densa decreases
Decreased concentration elicits response from macula densa
Response from macula densa has two effects
Dilation of afferent arteriole (increase glomerular hydrostatic pressure) (increase flow into glomerulus)
Stimulation of increased renin release from juxtaglomerular cells (increase constriciton)
Prevents major changes in GFR between MAPs of 75 to 160 mmHg
Myogenic Autoregulation
-strong increase in MAP then you see an increased afferent constriction
Problems With Juxtaglomerular Feedback
High protein intake
Higher than normal amino acid concentration in the blood – increase Na reabsorption -> increase in GFR and RBF when we don’t need one
-(20 to 30% increase in GFR 1 to 2 hours after eating a high-protein meal
Increase in blood glucose
-increase in glucose in the blood, glucose and Na reabsorption increase resulting in increase in GFR
The only way to change GFR is to change one or more of the forces driving filtration
Glomerular hydrostatic pressure (GP) (Primary Role)
Glomerular oncotic pressure (Gπ) (Secondary Role)
Bowman’s capsule (space) hydrostatic pressure (BP)
Bowman’s capsule oncotic pressure (Bπ)
what changes Glomerular hydrostatic pressure (Gp)
Mean arterial pressure
Afferent resistance***
Efferent resistance
what changes Glomerular oncotic pressure (Gπ)
Plasma protein concentration
Filtration fraction
what changes Bowman’s capsule (space) hydrostatic pressure (Bp)
Minimal change under normal physiologic conditions
Urinary tract obstruction
what changes Bowman’s capsule oncotic pressure (Bπ)
Minimal change under normal physiologic conditions
Changes in capillary permeability
Glomerular Hydrostatic Pressure (GP)
Mean arterial pressure
increase MAP : increase GP [will increase GFR ….countered by autoregulation*
Afferent resistance*
increase Afferent Resistance : decrease GP [will decrease GFR]
Efferent resistance
increase Efferent Resistance : increase GP [will increase GFR]
Glomerular oncotic pressure (Gπ)
Plasma protein concentration (PL π)
increase in PL π : increase Gπ [will decrease GFR]
Filtration fraction (FF)
increase FF : increase Gπ [will decrease GFR]
As the average Gπ increases, GFR will decrease
