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31 Cards in this Set
- Front
- Back
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Intrinsic changes in___________________ maintain constant RBF & GFR, with acute BP changes (renal artery pressure change)
Why is this necessary? |
vascular resistance
assures normal renal function & prevents damage to capillary bed during hypertension |
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The ________________ is the main site of renal autoregulation via vascular resistance
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afferent arteriole
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what are the 2 mechanisms for intrinsic autoregulation?
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1. Myogenic
(mediated by SAC) 2. Tubuloglomerular Feedback (TGF) (mediated by Juxtaglomerular Apparatus (JGA)) |
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Describe the Myogenic mechanism for intrinsic autoregulation
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changes in wall tension (mechanical stretch)-->
opens Stretch Gated Channels (SAC)--> Na+ & Ca+ flow into cell--> leads to vascular smooth muscle response--> contraction or relaxing |
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Describe the Tubuloglomerular Feedback (TGF) mechanism for intrinsic autoregulation
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high MAP, thus high RBF & GFR-->
activates NKCC2 transporters (macula densa)--> increases Na+ & Cl- in JGA)--> high Cl- leads to high [Cl-]intracellular--> activates nonselective cation channel--> increases [Ca2+]intracellular--> releases adenosine--> adenosine binds A1 receptor--> vascular smooth muscle contraction--> increases resistance of afferent arteriole--> decreases GFR |
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Intrinsic regulation of Na+ & Cl- transport is via __________________
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Glomerulotubular (GT) balance
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Describe GT balance
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When GFR decreases, ultrafiltrate flow rate decreases, and Na+ load is reduced
HOWEVER, a constant fraction of Na+ load is still reabsorbed by PT |
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Describe peritubular control of GT balance
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increased FF (GFR/RPF) -->
Hydroosmotic PC pressure decreases & oncotic PC pressure increase--> leading to reabsorption of fluid in peritubular capillaries--> decrease in plasma PC (if FF decreases, opposite occurs) |
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ECF Osmolality is NOT directly regulated, instead it is adjusting via _________________
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water intake & loss
(^changes ECF volume, thus changing Osmolality) |
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How is ECF Osmolality detected?
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via hypothalamic osmoreceptors
(detect change in shape, shrinkage when fluid loss) |
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Hypothalamic osmoreceptors communicate to neurosecretory cells to release ________
(also communicate w/ brainstem areas that regulate thirst) |
ADH/AVP
(ADH increased in response to high ECFosm = low water)) |
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Which is more tightly regulated?
water volume or osmolality |
water volume
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Na+ excretion is triggered by altered [Na+] or ECF volume?
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altered ECF volume
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High [Na+]plasma leads to
(increased/decreased) plasma omsolality which leads to increased ADH/AVP secretion |
increased plasma osmolality
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High [Na+]plasma leads to
(increased/decreased) ECF volume, which leads to (increased/decreased) Na+ excretion |
increased ECF volume
increased Na+ excretion |
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Baroreceptors sense low ECF volume & stimulate brain.
The brain illicits a sympathetic response and increases posterior pituitary to release _______ What does this result in? What does this result in? |
AVP/ADH
increased renal Na+ reabsorption & antidiuresis (urine concentration) to increase fluid volume |
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Describe how low ECF volume activates the RAA axis
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low ECF volume-->
low GFR--> low NaCl delivery to macula densa--> increased Renin--> conversion of angiotension to ANG I--> ANG I converted to ANG II (by ace)--> ANG II stimulates thirst & ADH/AVP & aldosterone release--> Increases water intake, decreases water & Na+ excretion--> increase in ECF volume |
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Renin production is also induced by _____________ & ____________
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increased sympathetics & decreased activation of stretch receptors in granular cells
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ANG II increases efferent arteriole resistance, what does this lead to?
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increased efferent arteriole resistance-->
decreased hydrostatic PC pressure & increased filtration fraction--> increased oncotic PC pressure (along w/ decreased hydrostatic)--> increased proximal Na+ reabsorption--> decreased Na+ & water excretion |
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ANG II decreases Vasa recta blood flow, what does this lead to?
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decreased vasa recta blood flow-->
increased urea in interstitium--> increased passive gradient in tAL--> increased tAL NaCl reabsorption --> decreased Na+ & water excretion |
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ANG II also increases NKCC2 transport, what does this do?
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increases Na+ reabsorption
(leading to decreased Na+ & water excretion) |
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What does increased aldosterone lead to?
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increased ENaC in principal cells (CCT)--> increased Na+ reabsorption
& increased Na/K pump activity |
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In moderate sympathetic tone increase, (afferent/efferent) arteriole resistance is increased more
In high tone (afferent/efferent) arteriole resistance is higher |
efferent (moderate)
afferent (high |
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efferent arteriole resistance increase ultimately leads to
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Na+ reabsorption
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afferent arteriole resistance increase ultimately leads to
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decreased water loss
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Moderate sympathetic tone increase also stimulates alpha-adrenergic receptors. What does this lead to?
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increases activity in Na/H exchanger (apical PT) & in Na/K pump (basolateral),
THUS increasing Na+ reabsorption |
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ANP is released in response to (high/low) ECF volume
What does ANP do? |
high ECF volume
vasodilates--> increased RBF & GFR--> incr. natriureis decreases Na+ reabsorption--> incr. natriuresis |
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Insulin, epinephrine, & aldosterone stimulate the Na-K pump to increase intracellular (Na/K)
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K
(this stabilizes extracellular K) |
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How does increased ECF volume affect K+ levels?
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leads to increased K+ secretion (kaliuresis)
(due to increased luminal flow) |
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How does increased Aldosterone affect K+ levels?
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leads to increased K+ secretion
(due to increased Na/K pump activity) |
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How does low K+ load (low dietary intake) lead to decreased K+ secretion?
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by increasing pH in alpha-intercalated cells, which increased K/H exchanger activity, increasing K+ IN
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