Test 2 (Regulation of Sodium and Water Balance) Flashcards Preview

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Flashcards in Test 2 (Regulation of Sodium and Water Balance) Deck (36):
1

Major Body Fluid Compartments

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

- Interstitial Fluid: Na+

- Plasma: Protein (Usually Albumin)


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

2

Electrolyte Compositions of ICF and ECF differ

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

3

Osmotic Eqilibration

- 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)

4

Total Body Na+ content determines ECF Volume

- 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!!!!!!!!

5

Sodium Balance

- 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!!!!!!!

6

Reabsorption of filtered Na+ Load

- Bulk of REABSORPTION of filtered Na+ in Proximal tubule, Loop of Henle; 'Fine Tuning' of Na+ handling is exerted in the Distal Nephron

7

Neurohumoral Factors controlling Renal Na+ Handling

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

8

Sympathetic activity stimulates Na+ Reabsorption, Renin Secretion

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

9

Factors that promote Renin Secretion

- 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

10

Angiotensin II Stimulates

- 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

11

Summary- Renal Effects of Angiotensin II

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

12

Response of Renin/ Angiotensin mechanism to Decreased ECF Volume

- 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

13

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

- Low Blood Pressure, Low Renal Blood Flow, and Catecholamines ACTIVATE Renin Secretion!!!!

14

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

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!!!!!!

15

Factors Controlling Aldosterone Secretion

1) INCREASE Plasma Potassium Concentration

2) ICNREASE Plasma ACTH Concentration

3) Volume Depletion

16

Feedback Control of Aldosterone Secretion

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

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

17

ANP Increases Na+, H2O Excretion

- 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

AANP Response to Increased ECF Volume

- INCREASED Extracellular Fluid Volume leads to DECREASED Tubular Sodium Reabsorption

- That then leads to INCREASED SODIUM EXCRETION!!!

19

Renal Response to Increased Blood Volume

- 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

Urodilatin: Endogenous Renal Natriuretic Peptide

- 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

Infrarenal Prostaglandins (Ex: PGE2) INCREASE Na+ EXCRETION

- 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

Summary- Nephronal NaCl Transport Mechanisms and Regulatory hormones

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

Anatomy of AVP Synthesis, Secretion

- HYPOTHALAMUS

24

Osmoreceptors, Baroreceptors Control AVP Secretion

Two major Stimuli for ADH Release:
1) HYPEROSMOLALITY

2) Volume Depletion


- Hypothalamic Osmoreceptors are MORE IMPORTANT than hepatic Osmoreceptors

25

Plasma AVP vs Osmolality, Blood Volume

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

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

- 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

Renal Response to Increased NaCl Intake

- 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

Integrated Response to Volume Expansion

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

Clinical manifestations of Impaired Regulation

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

Activation of Angiotensin II in response to Hemorrhage

- 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

Integrates Response to Hemorrhage

- 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

Increased Water Retention flowing Hemorrhage

- 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

Integrates Response to Volume Contraction

- Volume Contraction

---->

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

--->

- INCREASED ADH
- DECREASED Na=, H2O Excretion
- INCREASED Aldosterone

34

Increased Renal Tubular Na+ Reabsorption in response to Volume Contraction

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

Sensors and Effectors of Osmoregulation and Volume Regualtion

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

Summary

- 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