Sodium, Potassium and Volume Regulation
Key concepts linking sodium content, ECF volume, RAAS, aldosterone and natriuretic peptides.
Keyboard Shortcuts
💡 Pro tip: Use keyboard shortcuts for faster studying!
Study Smart Tips for Sodium, Potassium and Volume Regulation
Master these concepts using proven study techniques that actually work:
Active Recall
Test yourself before flipping each card to strengthen memory retention
Spaced Repetition
Review difficult cards more frequently than easy ones
Multiple Sessions
Break study time into shorter, focused sessions
Explain Aloud
Verbalize answers to reinforce understanding
Questions Covered in This Set
10 cards to master
What does total body sodium content determine?
Extracellular fluid (ECF) volume — and therefore blood pressure and tissue perfusion. Plasma Na⁺ concentration instead reflects water balance.
What is effective circulating volume (ECV)?
The portion of ECF actually perfusing tissues. In heart failure or cirrhosis, total ECF is high but ECV is low, so the kidney wrongly retains salt and water.
Name the three main volume-sensing sites.
1) JG cells of afferent arteriole (perfusion pressure), 2) macula densa (NaCl delivery via NKCC2), 3) cardiopulmonary/arterial baroreceptors (via sympathetic β₁).
Outline the RAAS cascade.
Renin from JG cells → angiotensinogen (liver) → angiotensin I → ACE (lung/renal endothelium) → angiotensin II → aldosterone from zona glomerulosa.
List the main actions of angiotensin II.
Systemic vasoconstriction; efferent arteriolar constriction (preserves GFR); stimulates proximal NHE3 Na⁺/HCO₃⁻ reabsorption; releases aldosterone; stimulates ADH and thirst.
How does aldosterone act on principal cells?
Via the mineralocorticoid receptor it increases apical ENaC, apical ROMK, and basolateral Na⁺/K⁺-ATPase → Na⁺ in, K⁺ and H⁺ out.
Phenotype of aldosterone excess vs deficiency?
Excess (Conn): hypertension, hypokalemia, metabolic alkalosis. Deficiency (Addison, spironolactone): hypotension, hyperkalemia, mild metabolic acidosis.
What triggers ANP and BNP release and what do they do?
Atrial stretch → ANP; ventricular stretch → BNP. Via cGMP: afferent dilation/efferent constriction (↑GFR), inhibit medullary collecting duct Na⁺ reabsorption, suppress renin, aldosterone and ADH.
What is pressure natriuresis?
A rise in arterial pressure raises renal interstitial hydrostatic pressure and washes out the medullary gradient, reducing Na⁺ reabsorption — the most powerful long-term controller of volume.
Why do ACE inhibitors drop GFR in bilateral renal artery stenosis?
GFR there depends on AT-II–mediated efferent arteriolar constriction; blocking AT-II dilates the efferent arteriole and drops glomerular filtration pressure.
