Regulation of Sodium and Water Balance Flashcards
Why do changes in Na+ balance alter ECF volume?
[Na+] affects osmolality, which determines fluid movement between ECF and ICF
Osmolality changes also alter thirst and ADH release, which alters volume
Effective circulating volume
Portion of ECF contained w/in vasculature that is perfusing tissues
How is ECV influenced by changes in Na+ balance?
ECV reflects the activity of volume receptors (heart), and thus Na+ balance
What are mechanisms by which the body monitors ECV?
Vasculature baroreceptors (low and high pressure)
Volume receptors (Atria and R ventricle)
Hepatic volume and [Na+] sensors
CNS [Na+] sensors (carotids and CSF
In low volume, what are the major signals acting on the kidneys to alter Na+ excretion?
Volume receptors (SNS)
Vascular baroreceptors (SNS and ADH)
TG Feedback (RAAS)
In high volume, what are the major signals acting on the kidneys to alter Na+ excretion?
Atrial distention (ANP)
Ventricular distention (BNP)
Vascular baroreceptors (less SNS and ADH, more parasympathetics)
TG feedback (?)
What are some major signals acting on the kidneys based on Na+ concentration to alter Na+ excretion?
Osmolality receptors (ADH)
Hepatic portal blood [Na+] receptors (SNS)
CNS [Na+] sensors (Ang2/NP’s)
How is NaCl intake/excretion related to ECF volume over time?
Why?
Over time, NaCl intake = isosmotic fluid intake (and vice versa)
Any changes in NaCl concentration will cause regulatory changes in water balance until ECF osmolarity is returned to normal, regardless of volume changes
When talking of ECF volume, what other volume-based concepts are directly related?
Vascular volume
Blood pressure
Cardiac output
CHF
Decreased BP and CO Baroreceptors cause ADH release Excess NaCl and H20 retained Increased ECF volume as a result Excess volume overflows into interstitium Edema
Hepatic cirrhosis
Portal vein blockage Venous return to heart decreased Venous pressure increased Decreased ECV and perfusion Baroreceptors cause ADH release NaCl/H20 retention causes edema
Unilateral renal artery atherosclerosis
Reduced renal perfusion pressure TG feedback RAAS Vasoconstriction Increased systemic BP Opposite kidney TG feedback (+Ang2 from 1st) Renin cut off Further water/Na loss Drop in BP
Effects of increasing SNS in the kidney
Constriction –> decrease GFR
Granular cells –> renin
PCT –> NaCl reabsorption (Starling)
Invoking the SNS in the kidney has what overall goal?
Restore ECF volume to normal (euvolemia)
What causes renin release? (3)
Low afferent perfusion pressure
Beta-adrenergics on granular cells (SNS)
TG feedback (low NaCl delivery)
How to inhibit renin release?
Intracellular calcium, ANP, NO, PGI2
The release of renin has what overall goal?
Maintain systemic arterial pressure for tissue perfusion
Functions of Ang II (5)
Aldosterone release (adrenal)
Vasoconstriction (increase BP)
ADH secretion + thirst (SFO and OVLT in brain)
Increased SNS (receptors in brain)
PCT NaCl reabsorption
Overall goals of Ang II?
Increase BP, decrease RBF, maintain GFR
Increase reabsorption
What causes the release of aldosterone? (2)
Ang II
Increased plasma [K+]
Function of aldosterone
NaCl reabsorption in the DCT/CD
Ionic exchange as a result of aldosterone
Cl- reabsorption
K+ / H+ secretion
What ions are affected by aldosterone?
Why?
Na, Cl, H, K
Increased Na/Cl symporter abundance
Increased apical Na+ permeability
Increased apical K+ permeability
Increased H+ ATPase in intercalated cells
What causes the release of natriuretic peptides?
What causes that?
Atrial/ventricular dilation
Volume expansion / heart failure
Function of natriuretic peptides
Relax vascular smooth muscle
Promote NaCl/H2O excretion
How do natriuretic peptides work?
Increase GFR and Na+ filtered load (afferent dilation, efferent const.)
Inhibit renin, aldosterone (direct and indirect), NaCl reabsorption (direct and indirect), ADH
What is the goal of Na+ reabsorption early in the nephron?
Constant delivery to DCT/CD for regulation
What is the goal of Na+ reabsorption in the late nephron?
Match NaCl intake, etc.
How does the proximal nephron maintain constant Na+ delivery to the late nephron? (3)
Autoregulate GFR (thus filtered load)
GT balance (PT load ∆ = PT reabsorption ∆)
Load-dependent reabsorption in Loop
In a volume expansion, what is the first goal of the body’s regulation?
What signal and effects start this?
Increase Na+ excretion
Volume sensors –> decrease SNS, increase NPs, inhibit ADH and renin and aldosterone
Results of vascular volume sensor and downstream effects in volume expansion (4)
Increase GFR
Increase Na+ filtered load
Decrease Na+ reabsorption in PT (Starling)
Decrease Na+ reabsorption in DT/CD (NPs + saturation)
When is ADH released?
Low volume (baroreceptors)
High osmolality (osmoreceptors)
Ang II stimulation in brain (SFO, OVLT)
ADH is released in volume depletion and osmolality increase.
When both are present simultaneously, how is ADH release affected?
Function of this?
Volume depletion –> lower osmolality necessary for ADH to be released
So ADH is released at a level below normal osmolality RATHER than only in HYPERosmolality
FUNCTION = get ADH going SOONER
Functions of ADH (4)
Vasoconstriction (SM)
Increased Na/K/Cl2 transporter action (TAL)
Increased urea reabsorption (CD)
Increased aquaporins (CD)
SIADH
Excess ADH release Excess H2O retention [Hyponatremia] Increased Na+ excretion (Starling) [MORE hyponatremia)
A patient is hypernatremic or hyponatremic. What is ALWAYS the cause?
Volume contraction or expansion
How does the body deal with excess sodium?
The excess causes a rise in ECF/ECV, which causes signal release for Na+ excretion
Diabetes insipidus (3 types)
Neurogenic - ADH doesn’t release
Nephrogenic - aquaporins don’t form
Gestational - abnormally low ADH in pregnancy
When is Na+ reabsorbed more than normal?
When ECF in decreased
How does FENa relate to ECV volume?
So?
Directly related
Low volume = low excretion
High volume = high excretion
What are the short term and long term effects of loop diuretics on renin release?
Short term – less Na reabsorption (TAL) = more delivery to DT = TG feedback = LESS renin
Long term – less delivery to DT because volume depletion = TG feedback = MORE renin
For a general renal injury, what is an acute (short term) time span?
What is a chronic (long term) time span?
Acute 2 days
Hyperaldosteronism
Increased Na+ reabsorption and K+ secretion = hypokalemia
Increased H+ ATPase (intercalated cells) = alkalosis
In a chronic state, why would a patient with high aldosterone or Ang II have low renin?
Negative feedback mechanisms on renin (aldosterone OR Ang II)
Urodilatin
Endogenous to kidney
Secreted by DT/CD due to increased ECF volume and arterial pressure
Function of urodilatin
Suppresses Na/H2O reabsorption in CD
How does urodilatin affect BP?
NO EFFECT
Local effect only
Intrarenal PGs
Increase GFR by dilating renal arterioles
Decrease reabsorption by increasing capillary flow
A patient has a disease in which an abnormal amount of intrarenal PGs are released (hyperactive COX-1). What is the renal danger of this disease?
Wash out medullary hyperosmolarity by inhibiting ion reabsorption
Trouble concentrating urine –> volume depletion
What is the danger of taking drugs that increase RBF?
Can inhibit the ability to concentrate urine
