Even small increases in arterial pressure often cause marked increases in urinary excretion of sodium and water, phenomena that are referred to as pressure natriuresis and pressure diuresis. Because of the autoregulatory mechanisms described in Chapter 26, increasing the arterial pressure between the limits of 75 and 160 mm Hg usually has only a small effect on renal blood flow and GFR. The slight increase in GFR that does occur contributes in part to the effect of increased arterial pressure on urine output. When GFR autoregulation is impaired, as often occurs in kidney disease, increases in arterial pressure cause much larger increases in GFR.
A second effect of increased renal arterial pressure that raises urine output is that it decreases the percentage of the filtered load of sodium and water that is reabsorbed by the tubules. The mechanisms responsible for this effect include a slight increase in peri-tubular capillary hydrostatic pressure, especially in the vasa recta of the renal medulla, and a subsequent increase in the renal interstitial fluid hydrostatic pressure. As discussed earlier, an increase in the renal interstitial fluid hydrostatic pressure enhances back-leak of sodium into the tubular lumen, thereby reducing the net reabsorption of sodium and water and further increasing the rate of urine output when renal arterial pressure rises.
A third factor that contributes to the pressure-natriuresis and pressure-diuresis mechanisms is reduced angiotensin II formation.Angiotensin II itself increases sodium reabsorption by the tubules; it also stimulates aldosterone secretion, which further increases sodium reabsorption. Therefore, decreased angiotensin II formation contributes to the decreased tubular sodium reabsorption that occurs when arterial pressure is increased.
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