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Renal I > Test 2 (Regulation of Sodium and Water Balance) > Flashcards

Test 2 (Regulation of Sodium and Water Balance) Flashcards

1
Q

Major Body Fluid Compartments

A

Main substances exerting Osmotic Pressure in Compartments:
- Cells: K+

  • Interstitial Fluid: Na+
  • Plasma: Protein (Usually Albumin)

**Values are for young adult male (70kg)

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2
Q

Electrolyte Compositions of ICF and ECF differ

A

Na+:

  • ICF = 12
  • ECF = 145

K+:

  • ICF = 150
  • ECF = 4

Ca++:

  • ICF = 0.001
  • ECF = 5

Cl-:

  • ICF = 5
  • ECF = 105

HCO3-:

  • ICF = 12
  • ECF = 25

Pi:

  • ICF = 100
  • ECF = 2

pH:

  • ICF = 7.1
  • ECF = 7.4
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3
Q

Osmotic Eqilibration

A
  • Osmotic Pressure determines the distribution of Body Water
  • Initially, ECF and ICF have same solute concentrations
  • Withdraw 3 liters pure H2O from ECF: OSMOTIC GRADIENT IS CREATED

OSMOTIC QUILIBRATION:
- H2O diffuses from ICF to ECF to re-establish Osmotic Equilibrium. Note proportional changes in each compartment’s volume (Look at slide8 in Lecture)

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4
Q

Total Body Na+ content determines ECF Volume

A
  • Water and Na balance are regulated INDEPENDENTLY by specific pathways designed to PREVENT LARGE CHANGES IN PLASMA OSMOLARITY
  • INCREASE Total Body Na+ Content
  • H2O Osmosis from cells, Renal H2O Retention
  • INCREASE Extracellular Fluid Volume

**Thus, INCREASED Na+ in the body expands the Extracellular Fluid Volume and effective Circulating Volume: CAN BE COMPENSATORY RESPONSE FOR HYPOVOLEMIA!!!!!!!!

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5
Q

Sodium Balance

A
  • PLASMA Na+ (and therefore Osmolarity) is regulated Primarily by changes in WATER BALANCE
  • TOTAL BODY Na+ CONTENT = Dietary Na+ intake - Urinary Na+ Excretion
  • Dietary Na+ intake is not regulated in humans; The kidneys control body Na+ content by adjusting Urinary Excretion
  • Increased ECF volume activates mechanisms that INCREASE Na+ EXCRETION
  • Decreased ECF volume causes Na+ to be CONSERVED!!!!!!!
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6
Q

Reabsorption of filtered Na+ Load

A
  • Bulk of REABSORPTION of filtered Na+ in Proximal tubule, Loop of Henle; ‘Fine Tuning’ of Na+ handling is exerted in the Distal Nephron
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7
Q

Neurohumoral Factors controlling Renal Na+ Handling

A

Factors that promote Na+ Reabsorption:
1) Activation of Renal Sympathetic Nerves

2) Activation of Renin/ Angiotensin System
3) Secretion of Aldosterone

Factors that promote Na+ Excretion:
- Release of Atrial, Brain Natriuretic peptides (ANP, BNP)

  • Release of Urodilatin
  • Interregnal Prostaglandins
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8
Q

Sympathetic activity stimulates Na+ Reabsorption, Renin Secretion

A

1) INCREASE Activity of Renal Sympathetic Nerves

——>

2a) DECREASE GFR
2b) INCREASE Proximal Na and H2O Reabsorption
2c) Direct Stimulation of Granular Cells (Beta Adrenergic Receptors)

——->

3) DECREASE Rate of Fluid Delivery to the Macula Densa

—–>

4) INCREASE Renin Secretion

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9
Q

Factors that promote Renin Secretion

A
  • RENAL SYMPATHETIC STIMUALTION (due to fall in Perfusion Pressure through the Cardiopulmonary BARORECEPTORS): Directly stimulates Renin secretion via B1 receptor activation in the JG apparatus
  • Tubuloglomerular Feedback: DECREASE NaCl delivery to MACULA DENSA ——> RENIN Secretion
  • Infrarenal Baroreceptor (Wall of afferent Arteriole): Afferent Arteriolar Vasoconstriction —–> INCREASE PRESSURE in Granular Cells ——–> RENIN Secretion
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10
Q

Angiotensin II Stimulates

A
  • Systemic Artfeiorlar Constriciotn
  • Renal Artfeiorlar Constriciton: Efferent > Afferent
  • Na+ Reabsorption: PCT (via INCREASE Na-H Exchanger Activity) > TAL, CCD
  • Thirst
  • ADH Secretion from Posterior Pituitary
  • Aldosterone Secretion from Adrenal Cortex
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11
Q

Summary- Renal Effects of Angiotensin II

A

1) Decreased Renal Blood Flow
2) Proportionately INCREASED Efferent Artfeiorlar Resistance —-> INCREASED Glomerular Capillary hydrostatic Pressure —–> Increased Filtration
3) Glomerular Mesangial Cell Contraction —-> DECREASED Glomerular Capillary surface area available for Filtration —-> DECREASED Filtration (offsets above effect)
4) DECREASED Medullary Blood Flow
5) INCREASED Tubular Sodium Reabsorption —> Sodium Retention

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12
Q

Response of Renin/ Angiotensin mechanism to Decreased ECF Volume

A
  • Angiotensin II DECREASED Medullary Blood Flow, INCREASES Renal Vascular Resistance, and INCREASED Aldosterone
  • An INCREASE in Renal Vascular Resistance causes a DECREASE in Renal Insterstitial Hydrostatic Pressure
  • All three of these cause an INCREASE in Tubular Sodium Reabsorption
  • This leads to a DECREASE in Sodium Excretion
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13
Q

Response of Renin/ Angiotensin mechanism to Decreased BP, RBF or release of Catecholamines

A
  • Low Blood Pressure, Low Renal Blood Flow, and Catecholamines ACTIVATE Renin Secretion!!!!
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14
Q

Aldosterones actions in late Distal Convoluted Tubule, Collecting duct (Principle Cells

A

1) Stimulates Sodium Reabsorption:
- Results in: Lumen-Negative Potential Difference

  • Electroneutrality maintained by: Passive Cl- Reabsorption and K+/ H+ Secretion
    2) Stimulates Potassium Secretion by Principal Cells of DT/ CCD
    3) Stimulates H+ Secretion (INCREASE H= - ATPase activity in Intercalated Cells of CCD)
  • *What would happen to K and H Excretion in a patient with Hyperaldosteronism?
  • Both would INCREASE!!!

***HYPOALDOSTERONISM: Hypokalemic and Alkalotic Patient Presentation!!!!!!

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15
Q

Factors Controlling Aldosterone Secretion

A

1) INCREASE Plasma Potassium Concentration
2) ICNREASE Plasma ACTH Concentration
3) Volume Depletion

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16
Q

Feedback Control of Aldosterone Secretion

A
  • Increased Renal Arterial mean Pressure and Decreased discharge of Renal Nerves INHIBITS-NEGATIVE FEEDBACK!!!!!!

***This all comes from DECREASED Na+ (and water) Excretion

17
Q

ANP Increases Na+, H2O Excretion

A
  • ANP Increases GFR: Afferent Arteriolar Dilation, Efferent Artieorlar Constriction
  • ANP INHIBITS Na+ Reabsorption in Medullary Collecting Duct
  • ANP SUPPRESSES Renin Secretion
  • ANP SUPPRESSES Aldosterone Secretion
  • ANP is a Systemic Vasodilator
  • ANP Suppresses AVP Secretion, Actions
18
Q

AANP Response to Increased ECF Volume

A
  • INCREASED Extracellular Fluid Volume leads to DECREASED Tubular Sodium Reabsorption
  • That then leads to INCREASED SODIUM EXCRETION!!!
19
Q

Renal Response to Increased Blood Volume

A
  • INCREASED in Circulating Blood Volume

——->

  • INCREASED Atrial Stretch

——–>

  • DECREASED ADH Secretion, DECREASED Aldosterone Secretion, DECREASED Renal Nerve Discharge, INCREASED Heart Rate

——>

  • All of these lead to INCREASED Salt and Water Excretion

——>

  • This leads to DECREASED CIRCULATION BLOOD VOLUME!!!!!
20
Q

Urodilatin: Endogenous Renal Natriuretic Peptide

A
  • SECRETED by DCT, Collecting Duct in response to INCREASED Arterial Pressure and ECF Volume
  • Urodilatin SUPPRESSES Na+ and Water Reabsorption by medullary Collecting Duct
  • Unlike ANP and BNP, Urodilatin has NO EFFECT on Systemic Circulation
21
Q

Infrarenal Prostaglandins (Ex: PGE2) INCREASE Na+ EXCRETION

A
  • INCREASE GFR by Dilating Renal Arterioles
  • Suppress Na+ Reabsorption in THICK ASCENDING LIMB, Cortical Collecting Duct
  • **What effect would this have on the Solute Concentration in the Renal Medullary Tissue?
    a) The concentration of solutes will DECREASE and there will be a DECREASED Osmolarity

b) This gets rid of the Gradient to REABSORB Sodium and Water and therefore we won’t be able to Concentrate our Urine
- Net effect: INCREASED Urinary Na+ EXCRETION!!!

22
Q

Summary- Nephronal NaCl Transport Mechanisms and Regulatory hormones

A

Percentage of Filtered NaCL Reabsorbed:

1) Proximal Tubule:
- 67%

2) Loop of Henle:
- 25%

3) Distal Tubule:
- 5%

4) Late Distal Tubule and Collecting Duct:
- 3%

23
Q

Anatomy of AVP Synthesis, Secretion

A
  • HYPOTHALAMUS
24
Q

Osmoreceptors, Baroreceptors Control AVP Secretion

A

Two major Stimuli for ADH Release:
1) HYPEROSMOLALITY

2) Volume Depletion
- Hypothalamic Osmoreceptors are MORE IMPORTANT than hepatic Osmoreceptors

25
Q

Plasma AVP vs Osmolality, Blood Volume

A

1) Plasma Osmolality:
- At 290 (Normal Osmolality) we have MAXIMAL ADH Secretion

  • Therefore the only thing that can fix the Osmolarity and Volume is THIRST

2) Blood Volume:
- Have to lose 10 to 15% of Bodys Plasma Volume before we see any INCREASE in ADG Plasma Volume

  • The system that senses Volume is NOT AS SENSITIVE as the Plasma Osmolality System. But is has a FASTER RISE in Plasma ADH Concentration!!!!
26
Q

Changes in Blood Volume modulate Osmolality- Dependent Changes in Plasma AVP

A
  • Volume depletion potentiates ADH response to Hyperosmolality
  • Volume depletion PREVENTS inhibition of ADH release normally induced by a Fall in Plasma Osmolality

***VOLUME is the STRONGEST STIMULUS for ADH release when eh Volume is LOWER!!!!!! (Too much Volume means less ADH released)

27
Q

Renal Response to Increased NaCl Intake

A
  • INCREASED Na Intake

—>

  • INCREASED EC Fluid Volume

—>

  • DECREASED Sympathetic Outflow to Kidney and ATRIAL STRETCH

—–>

  • DECREASED proximal Tubular NaCL Reabsorption and DECREASED NaCl Reabsorption in Collectin Duct

—–>

  • INCREASED Urinary NaCl Excretion!!!!!!!
28
Q

Integrated Response to Volume Expansion

A

Volume Expansion

—>

1) INCREASED ANP and BNP
2) DECREASED Sympathetic Activity
3) DECREASED Renin

—->

1) DECREASED ADH
2) INCREASED Na+, and H2O Excretion
3) DECREASED Aldosterone

29
Q

Clinical manifestations of Impaired Regulation

A

1) Too much Water - HYPONATREMIA (Low Plasma Na+)
2) Too little Water - HYPERNATREMIA (high Plasma Na+)
3) Too much Na+ - EDEMA
4) Too little Na+ - Volume Depletion

30
Q

Activation of Angiotensin II in response to Hemorrhage

A
  • Hemorrhage

—>

  • DECREASE Arterial Blood Pressure

—>

  • INCREASED Renin Secretion

—->

  • DECREASE RBF and GFR
  • INCREASED Tubular Sodium and Water Reabsorption

—>

  • DECREASED Renal Excretion of Sodium and Water
31
Q

Integrates Response to Hemorrhage

A
  • Hemorrhage

—>

  • DECREASED Aterial Blood Pressure

—>

  • INCREASED Sympathetic Outflow
  • DECREASED GFR
  • Infrarenal Baroreceptor
  • DECREASED ANP Secretion

—->

  • INCREASED Renin Secretion

—>

  • INCREASED Angiotensin II

—>

  • INCREASED NaCl Retention

—>

  • EC Volume Expansion

—>

  • Maintenance of Blood Pressure
32
Q

Increased Water Retention flowing Hemorrhage

A
  • Hemorrhage

—>

  • DECREASED Aterial Blood Pressure

—>

  • INCREASED NaCl Reabsorption
  • INCREASED Angiotensin II

—>

  • INCREASED ADH Secretion
  • Thirst

—->

  • INCREASED H2O Reabsorption from Collecting Duct
  • ICNREASED H2O Intake

—->

  • INCREASED Plasma Volume

—>

  • Maintenance of Blood Pressure
33
Q

Integrates Response to Volume Contraction

A
  • Volume Contraction

—->

  • INCREASED Sympathetic Activity
  • INCREASED Renin
  • DECREASED ANP and BNP

—>

  • INCREASED ADH
  • DECREASED Na=, H2O Excretion
  • INCREASED Aldosterone
34
Q

Increased Renal Tubular Na+ Reabsorption in response to Volume Contraction

A

Euvolemia:

  • 67% of Na+ Reabsorbed in PT
  • 25% of Na+ Reabsorbed in TAL
  • 1% of Na+ Excreted

Volume Contraction:

  • 80% of Na+ Reabsorbed in PT
  • 15% of Na+ Reabsorbed in TAL
  • 0 % of Na+ Excreted
35
Q

Sensors and Effectors of Osmoregulation and Volume Regualtion

A

OSMOREGULATION:

1) What is sensed?
- Plasma Osmolarity (Sensed in Brain)

2) Sensors:
- Hypothalamic Osmoreceptors

3) Effectors:
- ADH, Thirst

4) What is affected?
- Urine Osmolarity; Water Intake

VOLUME REGULATION:

1) What is sensed?
- Adequate Tissue Perfusion

2) Sensors:
- Macula Densa, Afferent Arterioles; Atria; Carotid Sinus

3) Effectors:
- RAAS; ANP; NE; ADH

4) What is affected?
- Urinary Sodium; Thirst

36
Q

Summary

A
  • Body fluid compartments; H2O equilibration across membranes
  • Neurhuxoral factors controlling Na+ Reabsorption: Sympathetic activity, Angiotensin II, Aldosterone, ANP, BNP, Urodilatin
  • Factors controlling AVP Secretion; Osmolarity, Blood Pressure
  • Integrated responses to Physiological Challenges

Renal I (14 decks)

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