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Kidney Lect 3

Renal Hemodynamics

QuestionAnswer
Renal Blood Flow (RBF) ammount of blood that perfuses both kidneys each minute (1200 ml/min)
Renal plasma flow (RPF) the rate of plasma flow to the kidneys each minute (670 ml/min). (About 55-60% of renal blood flow in a person with a normal hematocrit).
Glomerular Filtration Rate (GFR) the volume of plasma filtered each minute by the glomeruli. Normal GFR 125 ml/min for males and about 100 ml/min for females.
Filtration Fraction (FF) ratio of GFR to RPF (normally about .18-.22)
How does pre-glomerular blood flow vary by glomeruli? Pre-glomerular blood flow appears to be related to the size of the glomerulus. Thus, the larger juxtamedullary glomeruli (next to the junction of the renal cortex and medulla) have greater blood flow than the midcortical or superficial cortical glomerul
____ circulation varies in the kidney Regional
Post-glomerular blood flow a. 85% of post-glomerular blood flow goes to the cortex. b. 15% of post-glomerular blood flow goes to the medulla.
How does blood flow in the kidney change after getting a bolus of salt (e.g. meal high in protein or salt) Increased salt or other solute intake increases blood flow to the more superficial glomeruli that have shorter loops of Henle. The result of this redistribution would be to more efficiently excrete the excess solute.
____ is determined by the balance of hydrostatic and oncotic pressures (Starling principle); what equation describes this? GFR; GFR = Kf [(Pgc-Pb)-(Πgc-ΠB)]
K{f} glomerular coefficient or filtering capacity of the glomerular filtration barrier. Determined from the product of the total filtering surface area of the glomerulus times the hydraulic conductivity of the glomerular membrane.
P{gc} the glomerular capillary hydrostatic pressure, related to renal perfusion pressure and afferent and efferent arteriolar resistances.
P{b} the hydrostatic pressure within Bowman's space
Π{gc} the glomerular capillary oncotic pressure.
Π{B} the oncotic pressure in Bowman's space (negligible).
Constriction of the afferent arteriole (pre-glomerular) _____ afferent arteriolar resistance and ____ RBF, glomerular capillary hydrostatic pressure and GFR. increases, reduces
Constriction of the efferent arteriole (post-glomerular) ____ efferent arteriolar resistance _____ glomerular capillary hydrostatic pressure and GFR, while _____ RBF. increases, increasing, decreasing
Increased efferent arteriolar resistance also increases _____ ____ _____ pressures, increases the luminal hydrostatic pressure in the proximal nephron and favors salt and water reabsorption from the proximal tubule. peritubular capillary oncotic
How does dilation of the afferent arteriole affect: arteriolar resistance, RBF, flomerular capillary hydrostatic pressure, GFR? Dilation of the afferent arteriole decreases afferent arteriolar resistance, increases RBF, glomerular capillary hydrostatic pressure and GFR.
How does dilation of the efferent arteriole affect: arteriolar resistance, RBF, flomerular capillary hydrostatic pressure, GFR? Dilation of the efferent arteriole decreases efferent arteriolar resistance, increases RBF and decreases glomerular capillary hydrostatic pressure and GFR.
How does K{f} affect GFR? Increased Kf due to mesangial cell relaxation would increase GFR, while GFR would decrease if Kf decreased due to mesangial cell contraction.
Autoregulation he maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, and GFR) despite large changes in the systemic blood pressure
autoregulation is accomplished by adjusting ___ ___ resistances. renal vascular
The predominant regulatory changes in renal vascular resistance under normal conditions occur in _____ ____ ___. pre-glomerular "afferent" arteriole
Fundamental structural components of the glomerulus involved in autoregulation include: a. Afferent arteriole. b. Efferent arteriole. c. Macula densa. d. Glomerular mesangial cells. e. Sympathetic nervous system.
Bulk reabsorption of solute and water (about 90%) occurs in what structures? the proximal tubule and Henle’s loop
The final qualitative changes in urinary excretion occur in the ____ ____. distal tubules
The primary site of qualitative change is the ___ ___. collecting tubule
What happens if the nephrons are overloaded? Nephron segments have a limited total reabsorptive capacity. If delivery to these segments was not closely regulated, enhanced flow would overwhelm the reabsorptive capacity of distal segments. Result would be life-threatening losses of salt and water.
Describe the concept of Effective Circulating Volume a. Tight control of GFR and reabsorption by the kidney maintains Effective Circulating Volume. b. Effective circulating volume is defined as that volume necessary in the vascular space necessary to ensure adequate vital organ perfusion
Myogenic Hypothesis Arterial smooth muscle contracts and relaxes when vascular wall tension, respectively, increases or decreases; responses to wall tension appears to be mediated by Ca++ and are confined to the afferent arteriole, though sensing mechanisms unknown
How do arteriolar smooth muscle contractions autoregulate flow through the kidney? Increase in perfusion pressure distends renal arteriolar blood vessel walls and increases wall tension. --> contraction of resistance vessels --> decreases perfusion pressure and blood flow back toward normal values.
Tubuloglomerular feedback (TGF) TGF feedback is dependent on the close proximity of the specialized cells of the macula densa with the smooth muscle cells and granular cells of the juxtaglomerular apparatus.
By which mechanism does the macula densa help control changes to renal tubular flow? The macula densa cells detect changes in chloride delivery that occur with alterations in renal tubular flow. This results in appropriate changes in preglomerular arteriolar resistance.
How would the macula densa use chloride flow to help autoregulate GFR? Maybe due to the chloride dependence of the Na, K, 2 Cl pump in the luminal membrane of the cortical and medullary thick limbs of the loop of Henle. Osmolality of the luminal fluid may also play a role.
How would the macula densa respond to increased RBF? RBF increases-->GFR + fluid/solute delivery to tubule increase-->Macula densa see increased Cl- delivery-->signaling cascade in macula densa transmitted to the afferent arterioles--> vasoconstriction--> decrease RBF and GFR
The cellular message from the macula densa to the afferent arteriole is ____. unknown.
the tubular fluid constituent sensed by the macula densa is ____. chloride (appears to be)
Adenosine hypothesis: how are adenosine levels affected by tubular flow? as tubular flow increases ATP hydrolysis in the macula densa cells increases. This increases the local interstitial concentration of adenosine.
What's the relationship between adenosine and arteriolar constriction? The afferent arteriole has a high concentration of type 1 adenosine receptors. At these sites adenosine acts 35 as a potent vasoconstrictor. Such a mechanism would help reduce the delivery of solute to the macula densa.
When is the Renin-angiotensin system activated? This system is activated by many stimuli but the most important are connected to situations where volume homeostasis is compromised.
What is the function of the Renin-Angiotensin system? Stimulation of renin secretion and the subsequent production of angiotensin II maintain arterial blood pressure, renal perfusion pressure, preserve GFR, and minimize salt and water losses.
Renin: where is it stored? Where is it released? enzyme stored and synthesized in the granular epithelial cells of the afferent arteriole in the JG apparatus. Renin is released into the surrounding interstitium:
When is renin released? 1) Renal artery perfusion pressure decrease (decreased blood volume or decreased extracellular fluid) 2) when afferent arteriolar, carotid arterial and atrial wall tension decrease 3) increased Na+ intake 4) renal sympathetic nerve activity increases
What is the sensing mechanism that detects decreased blood volume and stimulates renin secretion? Sensing mechanism - renal vascular baroreceptor in the JG cells that appears to be directly sensitive to afferent arteriolar wall tension
How are changes in the afferent arteriolar, carotid arterial, and atrial wall tension detected? What happens when they are stimulated? Vascular baroreceptors in these sites activate the sympathetic nervous system and increase release of catecholamines. Catecholamines interact with adrenergic receptors in the afferent arteriole and increase renin release.
What intracellular signaling molecule appears to be responsible for renin secretion? The stimuli listed above appear to decrease intracellular calcium and increase cytosolic cyclic AMP levels in the juxtaglomerular cells, resulting in renin secretion.
What (4) molecules inhibit renin release? Renin release is inhibited by angiotensin II, potassium, antidiuretic hormone, and thromboxane A2.
What is the DIRECT action of renin? Renin actions and subsequent events - renin cleaves angiotensinogen (formed mainly in the liver) into an inactive angiotensin I (AI).
Once angiotensin I is synthesized, what happens? Next, Angiotensin converting enzyme (ACE) cleaves angiotensin I into biologically active, angiotensin II (AII)
Where are ACE and AII receptors found? Where is ACE activity found? ACE and AII receptors are found in most tissues but most AII in the systemic arterial blood is formed by ACE in the lungs. ACE is also found in the kidney.
What receptor is responsible for AII mediated effects? Most effects of AII appear to be mediated by the AII receptor subtype AT1.
How does AII arrive at its receptors throughout the body? AII arrives at renal vascular receptors via the circulation or by local cleavage of AI to AII by endothelial cell-bound ACE.
Is AII an endocrine or a paracrine? Both: AII plays a role as a circulating “endocrine” substance with systemic effects and as a paracrine/autocrine/intracrine substance with local effects that vary according to individual cell types
What effects does AII have in the kidney? 1) increase systemic BP and renal perfusion P 2)A+E-fferent arteriolar constriction (less GFR and RBF), net FF increase 3) mesangial cell contraction 4) aldosterone release, proximal Na+ absorption, thirst, sympat activity, antidiuretic hormone release
What seems to be the primary function of the renin-angiotensin system? The primary function of the renin-angiotensin system appears to be preservation of GFR during low perfusion states when RBF cannot be maintained
Prostaglandins fatty acid products of arachidonic acid that are synthesized within the kidney and act locally on renal vasculature as autocoids. Predominant in this group are PGE2, PGI2, and PGF2.
Prostaglandin synthesis and release are stimulated by ... renal vasoconstriction, volume depletion and renal hypoperfusion
What stimulates prostaglandin release? Prostaglandin release is stimulated by AII, bradykinin, catecholamines, antidiuretic hormone and glucocorticoids.
Endogenous prostaglandins regulate GFR and RBF by... direct afferent arteriolar smooth muscle action and indirectly by altering the action of neural and hormonal influences
How do prostaglandins help autoregulate blood flow in the kidney (in context of homeostasis)? The vasodilating effect of prostaglandins helps preserve renal blood flow in the presence of vasoconstrictors such as AII or the sympathetic nervous system.
How would the renin-angiotensin system and the syumpathetic nervous system react to actual volume depletion (e.g. hemorrhage) or perceived "effective" volume depletion (e.g. congestive heart failure or liver disease)? GFR and RBF both fall Subsequent release of prostaglandins causes afferent (pre-glomerular) arteriolar dilation resulting in decreased afferent arteriolar resistance, increasing RBF but with minimal effect on GFR.
If prostaglandin synthesis is inhibited by aspirin or nonsteroidal anti-inflammatory drugs in effective volume depleted states... ... vasoconstriction will be unopposed and renal function (waste removal, salt and water homeostasis) will be compromised as GFR and RBF fall.
What neural mechanisms control renal vasculature constriction/relaxation? Renal vasculature is richly innervated with adrenergic fibers of the sympathetic nervous system (SNS)
Renal nerve stimulation causes... increased renal vascular resistance due to afferent and efferent arteriolar vasoconstriction. Higher levels of stimulation cause a predominant effect on the afferent arterioles and decrease glomerular capillary pressure.
The vasoconstrictor effect is dependent on ___receptors. The final result of this stimulation is a ____ in RBF and GFR α1-adrenergic; decrease
Stimulation of renal efferent nerves also increases ____ release from the ____ cells leading to... renin; juxtaglomerular; ncreased angiotensin II production and vasoconstriction of the afferent and efferent arterioles. Prostaglandin formation is stimulated as a well.
Are renal nerves necessary for autoregulation of renal hemodynamics? Renal nerves are not necessary for efficient autoregulation of renal hemodynamics or for the tubuloglomerular feedback mechanism.
When is SNS enervation important in regulating renal blood flow? Vasoconstriction due to neural stimulation is present with severe stresses, such as hemorrhage, severe volume depletion, congestive heart failure or hypoxemia.
What are the dominant regulators of renal blood flow and GFR in the sodium replete state and over the "normal" blood pressure range Intrinsic mechanisms of autoregulation, myogenic responses and tubuloglomerular feedback
When do neural and hormonal mechanisms become more important in regulating kidney blood flow? With volume contraction and Na depletion the neural and hormonal mechanisms play a greater role as the decrease in renal perfusion worsens
Created by: karkis77 on 2011-09-28



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