Lecture 12: Regulation Of Na Excretion Flashcards by Serinna Singh

List the components of sodium regulation

ECV

Sensors:
Arterial + renal BRs
cardiopulmonary receptors

Effectors:
Urinary excretion
Nerves/hormones = sympathetic division, RAAS, ADH, ANP, vasodilator PGs

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What is total body sodium sensed by?

Surrogate =

ECV

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Define effective circulating volume (ECV; arterial filling)

Explain how it differs from ECF

ECV = the part of the ECF that can activate mechanisms to bring changes in sodium excretion

It’s the part of the ECF that is in the arterial system and can be sensed by regulatory mechanisms involved in sodium homeostasis

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Identify two diseases in which ECF and ECV are dissociated, explaining why total body sodium is increased in these diseases

HF
Nephrotic syndrome

Sensors detect decreased ECV (even though the ECF is actually increased) - sodium- retaining mechanisms get activated

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Describe effects of volume depletion on ECF, ECV and CO

ECF = dec.
ECV = dec.

CO = dec.
(Loss of vol. = dec. PL)

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Describe effect of HF on ECF, ECV and CO

ECF = inc.

ECV = dec.
(Less vol/stretch sensed leading to water/salt retention that will inc. ECF)

CO = dec.

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What are effects of nephrotic syndrome on ECF, ECV and CO

ECF = inc.

ECV = dec.

CO = no change or dec.

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Define pressure natriuresis, briefly describing the proposed mechanisms for this effect

Phenomenon of BP’s direct effect on sodium excretion

Mediated mainly by dec. Na reabsorption

When there is inc. Na intake (and more total body sodium), ECV inc. = inc. BP = inc. renal perfusion pressure = dec. Na reabsorption and inc. GFR = inc. sodium excretion

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Describe the effect of increased nerve traffic on kidney function/sodium excretion

Nerves and hormones speed up sodium balance and decrease impact of dietary salt on total body sodium

Dec. ECV = dec. stretch of arterial BRs = inc. symp. Tone to kidneys
+ inc. sodium reabsorption
+ inc. renin secretion
+ as a last resort: dec. GFR

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Describe innervation of kidney

EXCLUSIVELY sympathetic

3 main innervated:
+ AA
+ granular cells
+ tubular epithelium

Receptor subtypes:
alpha1, alpha2, beta1

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Describe effect of low levels of sympathetic stimulation

Alpha2 receptors on PT + beta on DCT get stimulated

Inc. NHE in PT
=
Inc. Na reabsorption in PT and inc. Na reabsorption in DCT via NCC

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Describe effect of intermediate levels of sympathetic stimulation

Beta1 receptors on granular cells stimulated

Inc. renin secretion
=
Activation of RAAS
=
Inc. Na reabsorption AND renovascular effects

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Describe effect of high levels of sympathetic stimulation

“Last resort of neural regulation”

Alpha1 on AA stimulated
=
Vasoconstriction
=
Dec. RBF and GFR

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Describe indirect/direct relationships amongst effectors of sodium homeostasis

ECV + arterial BRs = direct

arterial BRs + symp. Tone = indirect

Symp. Tone + sodium excretion = indirect

Symp. Tone + RAAS = direct

RAAS + sodium excretion = indirect

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What are hormonal regulators of Na balance and ECV?

Vasoconstrictors + anti-natriuretic hormones:
+ AngII
+ Aldosterone
+ Vasopressin (ADH)

Vasodilators + natriuretic hormones:
+ ANP/BNP
+ PGs
+ NO

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Describe effects of AngII on systemic circulation, renovascular, and tubules

Systemic circulation:
Vasoconstriction = Inc. SVR = inc. BP

Renovascular:
More vasoconstriction on EA than AA = dec. RPF & inc. GC hydraulic pressure = inc. FF & ____ effect on GFR

PT: inc. Na reabsorption via NHE

DCT/CNT/CD:
Inc. aldo and direct stimulation of NCC and ENaC = inc. Na reabsorption

For volume depletion, what are pattern of RAAS components in the plasma?

Dec. stretch on arterial and intracranial BRs from depletion
=
Inc. renin secretion
=
Inc. AngII
=
inc. aldosterone

What are effects of PGs on kidney function?

Systemic circulation
Renovascular
Tubules

Counteract neurohormonal vasoconstriction

systemic circulation:
Local vasodilation = dec. SVR = dec. cardiac AF and BP

Renovascular:
Vasodilation @AA = inc. RPF + GFR

Thick AL and CD:
Dec. Na reabsorption (in humans?)

What increases PG synthesis?

Neurohormonal activation:

AngII
ADH
Sympathetic stimulation

What effect do PGs have on renin?

Inc. renin secretion

What effect can NSAIDs have when there is nerurohormonal activation?

Dec. renal perfusion and GFR

Little effect on renal fxn under normal conditions

Describe effect of ACEI on glomerular hemodynamics

ACEI = dec. synthesis of AngII = AA and EA vasodilation (EA&raquo_space; AA = dec. GC hydraulic pressure) = dec. RVR = inc. RPF

What does vasopressin do?

Allows reabsorption of water in CNT/CD

What regulates ADH secretion?

P(osm) and ECV

Inc. P(osm) = inc. ADH

Dec. ECV = inc. ADH

What are non-osmotic stimuli ?

High levels of AngII Severe vomiting, pain + major stress (post-op) Significant decrease in ECF or ECV

Describe relationship between osmotic and non-osmotic stimuli

Osmotic stimulus more potent vs. non-osmotic Strong non-osmotic can OVERRIDE osmotic

Describe effects of high levels and any levels of ADH

High levels = systemic circulation: ADH = V1 vasoconstrictor = inc. SVR = inc. BP any level = CNT/CD: Binding to V2 receptor on principal cells = insertion of AQP2 channels on apical side = inc. water reabsorption = dec. water excretion

What do osmoregulation and volume regulation sense? What do they affect?

Osmoregulation Sense: plasma osmolality Effects: water excretion (via ADH) + water intake (via thirst) Volume regulation Sense: ECV Effects: sodium excretion

Describe effects of ANP/BNP on systemic circulation, renovascular effects, and tubules

Systemic circulation: Vasodilation = dec. SVR = dec. cardiac AL Renovascular: Dilate AA + constrict EA = inc. GC hydraulic pressure, inc. RPF = inc. GFR = dec. renin secretion CD (IMCD): Oppose actions of aldosterone = dec. Na reabsorption

What are NO actions in the kidneY?

Vasodilation and inc. GFR Inc. Na excretion

Describe circumstances in which it is dangerous to administer an NSAID

True volume depletion or low ECV Examples: HF or cirrhosis

What is TGF?

Tubuloglomerular feedback Negative feedback system in kidney Macula densa senses salt delivered to alter GFR in the same nephron

Describe proposed mechanisms for TGF

Sense: Macula densa cells sense NaCl via NKCC2 while cilia sense flow Effects: Paracrine mediators constrict/dilate AA to induce change in GFR

What are effects on GFR of inc. NaCl delivery to macula densa?

Release of paracrine mediators (inc. adenosine) = AA constriction = Dec. GFR

What are effects of dec. NaCl delivery to macula densa?

``` Release of paracrine mediators (Dec. Adenosine, inc. PGE2) = AA dilation = Inc. GFR ```

Explain why TGF stabilizes the function of the nephron but does not stabilize TB sodium

TGF autoregulates GFR in single nephrons!!! Will affect distal nephron that shares same macula densa

Describe glomerulotubular balance (GTB) and the proposed mechanism for it

Describes positive relationship between tubular fluid flow rate and reabsorption Inc. in GFR + filtered load = inc. reabsorption of solutes (mainly PT) so that fraction of solute reabsorbed remains constant

What is GTB mediated by?

Physical factors Flow-mediated changes by microvilli on apical surface of PT