Kidney in hypertension: guyton redux

TM Coffman, SD Crowley - Hypertension, 2008 - Am Heart Assoc
TM Coffman, SD Crowley
Hypertension, 2008Am Heart Assoc
The RAS has potent actions to modulate pressurenatriuresis relationships in the kidney, 20,
21 and these actions shape the characteristics of RAS-dependent blood pressure regulation
in normal physiology and in disease states. For example, chronic infusion of Ang II causes a
shift of the pressure-natriuresis curve to the right, suggesting that when the RAS is activated,
higher pressures are required to excrete an equivalent sodium load. 20 Conversely,
administration of ACE inhibitors or Ang receptor blockers shifts the curve to the left, meaning …
The RAS has potent actions to modulate pressurenatriuresis relationships in the kidney, 20, 21 and these actions shape the characteristics of RAS-dependent blood pressure regulation in normal physiology and in disease states. For example, chronic infusion of Ang II causes a shift of the pressure-natriuresis curve to the right, suggesting that when the RAS is activated, higher pressures are required to excrete an equivalent sodium load. 20 Conversely, administration of ACE inhibitors or Ang receptor blockers shifts the curve to the left, meaning that natriuresis is facilitated at lower levels of blood pressure. The basic features of endogenous control of the RAS are consistent with these homeostatic functions. The system is activated at low levels of salt intake stimulating renal sodium reabsorption and conservation of body fluid volumes and blood pressure. In contrast, with high sodium intake, the system is suppressed, facilitating natriuresis. Direct evidence for the powerful capacity of renal excretory functions to modulate blood pressure in humans is provided by the genetic studies of Lifton et al. 22 In a series of elegant articles, these investigators have shown that virtually all of the Mendelian disorders with major impact on blood pressure homeostasis are caused by genetic variants affecting salt and water reabsorption by the distal nephron. 22 On the other hand, this concept has been challenged recently, and several recent studies have suggested that primary vascular defects may cause hypertension by impacting peripheral resistance without direct involvement of renal excretory functions. 23–26 However, in each of these studies, it is possible that renal vascular function might have been affected, consequently modifying the pressure-natriuresis mechanism and thereby raising blood pressure through a primary mechanism involving altered salt and water excretion by the kidney.
Am Heart Assoc