Physiology 2 Renal Blood Flow Flashcards
Renal Blood flow avereages what percentage of the cardiac output
20% (1000 ml/min)
Discuss the perfusion of kidneys relative to their metabolic needs. What is the significance
Over perfused for their metabolic needs - important in filtration function and cleansing the palsms
Renal oxygen consumption
linear relationship between renal oxygen consumption and Na+ reabsorption (90% of renal energy expenditure is devoted to the reabsorption of Na)
What is the principle transport system of Na in the kidney
Na K ATPase - located in the basolateral membranes of tubules (3Na out 2 K in )Important for maintaining low intracellular sodium concentrations (establishes Na gradient for the transport of other molecules)
Glomerular and Peritubular Capillaries are arranged in series/parallel
Series- glomerular capillaries arise from afferent arterioles and are continuous with efferent arterioles which give rise to the peritubular capillaries
Glomerular capillary starling forces
Favors filtration (capillary pressure >oncotic pressure)
Peritubular capillary starling forces
Favors reabsorption (oncotic pressures > hydrostatic pressure)
Autoregulation of RBF and GFR
60-100 mmHg. INTRINSIC PROPERTY. Uncouples changes in flow and GRF due to changes in arterial pressure (allows kidney to do its job despite flux in arterial pressure) Because blood flow is regulated so is GFR
Pressure diuresis
as the arterial pressure increases urination increases
Myogenic Vasoconstriction
Afferent arterioles. Increased pressure causes vessel to stretch resulting in myogenic vasoconstriction (protects the glomerular capillaries and decreases glomerular pressure) aka INTRA-RENAL BARORECEPTOR
Tubuloglomerular Feedback
Macula Densa in the distal nephron senses changes in flow and solute (Cl-) delivery- if GRF is too high the increased CL- flow results in vasoconstriction of the afferent arteriole to decrease RBF and GFR also inhibits renin release via ATP . If GFR is too low: leads to vasodilation to increase RBF and GFR and increase renin release via prostaglanding and NO
after the loop of henle how much of the filtrate has been reabsorbed
85%
Autoregulation of GFR with respect to autoregulation of blood flow
autoregulation of GFR is secondary to the autoregulation of blood flow
importance of extrinsic control of RBF and GFR
can override the intrinsic control
Extrinsic control of RBF and GFR: Neural control
Resting sympathetic tone is low. Constriction of the afferent arterioles decreases BOTH GRF and RBF. SHUNTS BLOOD AWAY FROM THE KIDNEY to help maintain arterial pressure and tissue perfusion
Extrinsic control of RBF and GFR: Humoral control
Vasoconstrictors (catecholamnes, angiotensin II, ADH, adenosine) are modulated by vasodilators (prostaglandns, kinins, APT, NO) to protect the kidney from extreme vasoconstriction resulting in ischemia and decreased GFR
What is the importance of vasodilators in extrinsic humor control of RBF and GFR
modulates areterial tone in the face of vasoconstriction to protect the kidney from extreme ischemia and decreased GFR. CLINICAL COMMENT: Problem for patients in a chronic hypovolemic state (causes SNS vasoconstriction) who take NSAIDS (inhibits prostaglandins) - can lead to renal failure
What is the limiting element on the glomerular filtration barrier
the basement membrane
Why doesn’t albumin get through the Glomerular Capillary
Negatively charged membrane repels the negatively charged plasma protein. CLINICAL COMMENT: Nephrotic Syndrome causes loss of negative membrane and results in loss of plasma protien through the urine
Ultrafiltrate
“Everything except the plasma proteins”
Ultrafiltration
High glomerular hydrostatic pressure (PG) results in high rates of fluid filltration (GFR) BULK FLOW NOT DIFFUSION. Ultrafiltrate enters Bowman’s capsule and flows into the proximal tubule
What is not filtered in ultrafiltration
Plasma proteins, substances bound to proteins(50% of Ca is bound to protein) , and formed elements (platelets)
Determinants of Glomerular Capillary Barrier Permeability
1.) The size and numer of membrane pores 2.) Presence of fixed negative charges on glomerular capillaries (negatively charged glycoproteins)
Average GFR
125 ml/min (~180 L/day)
How does glomerular capillary oncotic presure change
starts at 25 mmHg (same as systemic) and then increases along the capillary - due to the amount of fluid filtration from the glomerular capillaries causes plasma protiens to become more concentrated
What happens to GFR as you increase renal plasma flow
increase GFR
glomerular capillary filtration coefficient compared to systemic capillaries
50-100 times greater than systemic (a lot leakier) - due to resistance on either side of the capillary bed
what is the driving force for flow through the nephron
The Hydrostatic pressure in Bowman’s space (PB)
Peritubular capillaries
specialized for uptake of reabsorbed fluid and solutes from interstitium. Close proximity to renal tubules. Low Capillary pressure and high onoctic pressure favors reabsorption (as filtration fraction increases the oncotic pressure in peritubular capillaries increases more)
What is the effect of Efferent aretriolar vasoconstriction on the peritubular capillaries
increase in plasma oncoti and decrease in plasma hydrostatic in the peritubular capillaries = becomes more favorable for the absorption of fluid (imprtant for enhancing net proximal tubular reabsorption in hypovolemic states)
Back- leak
Seen in hypervolemic states when there is affernet and efferent arteriolar vasdilation leading to decreased FF (GFR/RPF). Reabsorption becomes less favorable - not taken up by peritubular capillaries and there is a progresisve rise in interstitial hydrostatic pressure causing fluid to leak BACK into the proximal convoluted tubule by bulk flow (possible due to relatively leaky junctions in the PCT)
Changes in GFR and RBF (relative to one another)
Tend to change in the same direction. Magnitudes of chane will be differnet- typically GFR changes LESS than RBF due to changes in the efferent arteriole
Hypovolemia (GFR and RBF)
1.) Decreased MAP will decrease RBF and GFR (small due to autoregulation) 2.) Constriction of the afferent and efferent arterioles (increased synpathetic nervous system) 3.) increased plasma oncotic pressure in sympathetic capillaries (eg: dehydration) 4.) Decreased Kf (decreased surface area, contraction of mesangial cells and podocytes- reach filtration equilibrium sooner- less “effective surface area” ) = result: decrease in GFR and large decrease in RPF resulting in and increased filtration fraction
Changes in filtration fraction in hypovolemic states
constriction of BOTH the afferent and efferent arterioles leads to large decrease in RPF and smaller decrease in GRF resulting in an increased FF
What is the significance of an increased Filtration fraction
Filtration fraction is the proportion of fluid reaching the kidneys that passes into the renal tubules. When blood flow is reduced the filtration must increase in order to perform the normal tasks of the kidney in balancing fluid and electrolytes in to body (higher filtration fraction = kidney has to do more work with the fluid they are recieving)
Hypervolemia (GFR and RBF)
1.) Increased MAP will increas RBF and GFR (small due to autoregulation 2.) Dilation of afferent and efferent arterioles 3.) Decreased systemic plasma oncotic pressure (dilution) 4.) Increased Kf (relaxation of mesangial cells, increasd RBF causes equilibrium to be reached later- more surface area) Result= Increased RPF, Increased GFR and decreased FF
How does filtration equilibrium change with renal blood flow
increased renal blood flow causes equilibrium to be reached later. Decreased renal blood flow causes equilibrium constant to be reached sooner
