Hypertension in chronic renal failure.

Ten years ago, it was recognized by several groups [3, 7, 14, 18] that in many hypertensive patients with terminal renal failure long-term hemodialysis would normalize the blood pressure. Subsequent investigations showed that, whereas a majority of cases would respond favorably to removal of fluid and sodium (“controllable” hypertension), a minority would not (“uncontrollable” hypertension). More recently, there has been some controversy about the role of two possible mechanisms of hypertension in renal failure, volume-hypertension and vasoconstrictor-hypertension. In this respect oversimplification may be misleading, since the dynamics of blood flow cannot be interpreted in the light of static concepts. Overfilling of an elastic tubing with fluid undoubtedly increases the pressure inside, if there is no outflow. But the arterial part of the vascular system opens into the capacitance vessels. Thus, overfilling of the system only increases the venous pressure. The increased venous return to the heart results in an elevation of the cardiac output, but only up to a critical level and in the absence of heart failure. If there is no active change in the cross section of the arterial tree and blood viscosity remains unaltered, an increase in cardiac output produces a corresponding elevation of the blood pressure.