The long-term regulation of blood pressure is determined primarily by renal pressure natriuresis. According to the Guyton model, why can neurohormonal or vascular mechanisms alone NOT permanently raise blood pressure without renal involvement?

• A The sympathetic nervous system desensitizes after 48 hours of sustained activation, preventing long-term vasoconstriction from maintaining elevated blood pressure
• B The baroreceptor reflex is the primary long-term regulator; sustained activation of carotid baroreceptors permanently reduces sympathetic tone to normalize BP
• C Angiotensin II has a direct anti-natriuretic effect that reduces renal perfusion pressure, preventing the kidney from participating in long-term pressure control
• D Any sustained rise in arterial pressure increases renal perfusion pressure, raising GFR and sodium excretion until extracellular volume falls and cardiac output returns to baseline, resetting mean arterial pressure downward ✓

Explanation

Guyton's infinite-gain principle of renal-body fluid pressure control states that the kidney is the ultimate determinant of long-term arterial pressure. For any stable (chronic) blood pressure, the kidneys must be in sodium balance: intake = output. If any factor raises systemic BP, the elevated renal perfusion pressure increases sodium and water excretion (pressure natriuresis), contracting extracellular volume and cardiac output until BP normalizes. This means neurohormonal factors (angiotensin II, sympathetics) can only sustain hypertension if they simultaneously reset the pressure-natriuresis curve to a higher pressure set-point — either by directly reducing renal function or by shifting the curve rightward. This is why primary hypertension always involves abnormal renal pressure-natriuresis.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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