What is the main mechanism by which the kidney maintains stable glomerular filtration rate across a wide range of blood pressures?

• A. Afferent arteriolar myogenic response and tubuloglomerular feedback
• B. Decreased sympathetic tone
• C. Efferent arteriolar vasoconstriction
• D. Renin-angiotensin system activation

Answer: (A)

The kidney keeps GFR steady over a wide range of blood pressures through intrinsic autoregulation of the glomerular vessels, mainly via two local mechanisms: the afferent arteriolar myogenic response and tubuloglomerular feedback.

The myogenic response helps match filtration to incoming pressure: when arterial pressure rises, the smooth muscle in the afferent arteriole stretches and constricts, limiting the increase in glomerular capillary pressure and GFR. When pressure falls, less stretch leads to dilation, helping to preserve GFR. This quick, automatic adjustment occurs right at the input to the glomerulus.

Tubuloglomerular feedback provides a flow-and-NaCl-sensing check from the distal tubule. The macula densa detects how much NaCl is reaching the distal nephron. If delivery is high (reflecting high GFR), it signals the afferent arteriole to constrict (and can modulate nearby efferent tone) to reduce GFR. If delivery is low, it signals dilation to raise GFR. This feedback fine-tunes filtration to keep it stable despite changes in blood pressure.

The other options reflect systemic or hormonal influences that can modify GFR but do not explain the primary, rapid, intrinsic mechanism that maintains GFR across a wide BP range. Systemic sympathetic tone, while capable of lowering GFR during stress, is not the mechanism for constant GFR under normal fluctuating pressures. Efferent arteriolar vasoconstriction and renin-angiotensin system activation can alter GFR, especially during hypoperfusion, but they are not the foundational autoregulatory processes that sustain GFR across most physiological BP changes.