The ability of the kidney to increase sodium and water excretion in response to increases in perfusion pressure has been recognized for more than 50 years. Because glomerular filtration rate is tightly autoregulated, pressure natriuresis occurs as the result of decreased tubular sodium reabsorption rather than increased filtered load. Micropuncture and microperfusion data support the contention that acute changes in arterial pressure can alter proximal tubule reabsorption; however, studies have failed to show a consistent association between changes in sodium excretion and peritubular, interstitial, or tubular pressures. Thus, the specific intrarenal mechanism for the change in tubular reabsorption in response to an acute change in arterial pressure does not appear to be related to the peritubular physical factors at the level of outer cortical nephrons. The possible roles of angiotensin and prostaglandins as humoral mediators of pressure natriuresis are considered in this report. Although angiotensin II is a powerful modulator of the slope of the pressure natriuresis relationship, the responsiveness of sodium excretion to arterial pressure is actually enhanced by angiotensin-converting enzyme inhibitors. These data suggest that angiotensin does not mediate the basic phenomenon. Recent experiments indicate that intrarenal prostaglandins also modulate the magnitude of the pressure natriuresis relationship, but these hormones do not appear to be essential for its basic manifestation.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1986|
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