The role of renal interstitial pressure on the chronic control of arterial blood pressure

Several lines of evidence support the hypothesis that the kidney is involved in the generation and maintenance of arterial hypertension. The evidence comes from: 1) experimental models of hypertension showing that induction of all secondary forms of hypertension require some maneuvers to reduce the renal sodium and water excretion; 2) the existence of several rat models with genetic hypertension exhibiting a shift of the pressure-natriuresis relationship toward higher pressures; 3) renal transplantation experiments between normal and genetically hypertensive rats showing that hypertension follows the kidney; and 4) human genetic disease with chronic changes in arterial blood pressure levels in which all identified genes so far are part of a common pathway for renal sodium reabsorption. It is well known that pressure-natriuresis is the mechanism by which any changes in arterial pressures are followed by changes in renal sodium excretion. However, it has been recognized now that the interstitial pressure in renal medulla is the linkage between arterial pressure levels and the amount of sodium reabsorption. Thus, the medullary interstitial pressure might be involved in the long-term control of systemic arterial pressure. Part of these new lines of evidence associating the renal medullary interstitial pressure in the control of arterial pressure are due to the availability of new methods such as laser-doppler flowmetry and videomicroscopy, that allows the measurement of blood flow in renal cortex and medulla separately. Several studies with this methodology show that medullary, but not cortical presure and blood flow correlate positively with natriuresis. What still remains unsolved is the mechanism by which renal sodium reabsorption increases or decreases after changes in the medullary interstitial pressure occur.