myogenic response

**Mechanism:** Increased arterial pressure stretches the vessel wall, which activates mechanosensitive (stretch-activated) cation channels on vascular smooth muscle. This causes depolarization, opening of voltage-gated L-type Ca2+ channels, Ca2+ influx, and vasoconstriction. The increased resistance offsets the higher pressure, so flow stays constant. Decreased pressure produces the opposite effect: less stretch, less Ca2+ entry, vasodilation.

**Renal significance (high-yield):** - The myogenic response is one of two main mechanisms of renal autoregulation. The other is tubuloglomerular feedback (TGF). - It acts at the afferent arteriole and responds within seconds. - Renal blood flow and GFR stay relatively constant across a mean arterial pressure of about 80–180 mmHg. - Below about 80 mmHg or above about 180 mmHg, autoregulation fails, and RBF/GFR become pressure-dependent. - TGF is slower. The macula densa senses NaCl delivery, and when delivery is high it releases adenosine, which constricts the afferent arteriole.

**Other organs:** The myogenic response also contributes to autoregulation in the brain (cerebral autoregulation, with MAP roughly 60–150 mmHg), the heart (coronary), and skeletal muscle. It is not the dominant autoregulatory mechanism in these tissues, where metabolic factors (CO2, H+, adenosine, K+, O2) are also major.

**Clinical correlations:** - **Hypotension or shock:** When MAP drops below the autoregulatory range, GFR falls, causing prerenal AKI. - **NSAIDs:** They inhibit prostaglandin-mediated afferent dilation, which impairs autoregulation. Combined with volume depletion, this can cause AKI. - **ACE inhibitors/ARBs:** They dilate the efferent arteriole, so GFR falls when renal perfusion is low (e.g., bilateral renal artery stenosis). - **Chronic hypertension:** Autoregulation curves shift to the right in the brain and kidney. Rapid BP lowering can then cause hypoperfusion, which is why BP is lowered gradually in hypertensive emergency. - **Hypertensive nephrosclerosis and diabetic nephropathy:** Impaired afferent myogenic tone transmits systemic pressure to the glomerulus, causing hyperfiltration and glomerular injury. - **Calcium channel blockers:** Dihydropyridines (e.g., amlodipine, nifedipine) block L-type Ca2+ channels, dilating the afferent arteriole and blunting the myogenic response.

**Key distinction:** Myogenic response = intrinsic, pressure-sensing, fast, vascular smooth muscle. Tubuloglomerular feedback = macula densa, flow/NaCl-sensing, slower. Both are independent of extrinsic neurohormonal control.