Renal Autoregulation of GFR Renal autoregulation is effective for a systolic blood pressure range of 80 to 170 mmHg but cannot compensate for extreme BP variations. Renal autoregulation has two major mechanisms: myogenic and tubuloglomerular feedback. The myogenic mechanism is the result of stretching of the afferent arterioles due to higher blood pressures. Increased BP (which increases GFR) stretches the afferent arteriole. As a result, the smooth muscles of the afferent arteriole contract, constricting the arteriole, decreasing the amount of blood and the BP entering the glomerulus, and restoring the GFR. The second mechanism relies upon the fact that as GFR changes, the concentration of the tubular filtrate also changes (increased GFR decreases salinity and decreased GFR increases salinity). Special cells in the wall of the DCT close to the glomerulus, called macula densa cells, monitor the tubular fluid and signal juxtaglomerular cells to constrict or dilate the afferent arteriole (adjusting GFR accordingly). Regardless of which mechanism is
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