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Chronic Blood Pressure Control

Michael W. Brands

10.1002/cphy.c100056

Source: Volume 2, Issue 4, October 2012

Published online: October 2012

Full Article on Wiley Online Library



Abstract

Chronic blood pressure is maintained within very narrow limits around an average value. However, the multitude of physiologic processes that participate in blood pressure control present a bewildering array of possibilities to explain how such tight control of arterial pressure is achieved. Guyton and Coleman and colleagues addressed this challenge by creating a mathematical model that integrated the short‐ and long‐term control systems for overall regulation of the circulation. The hub is the renal‐body fluid feedback control system, which links cardiac function and vascular resistance and capacitance with fluid volume homeostasis as the foundation for chronic blood pressure control. The cornerstone of that system is renal sodium excretory capability, which is defined by the direct effect of blood pressure on urinary sodium excretion, that is, “pressure natriuresis.” Steady‐state blood pressure is the pressure at which pressure natriuresis balances sodium intake over time; therefore, renal sodium excretory capability is the set point for chronic blood pressure. However, this often is misinterpreted as dismissing, or minimizing, the importance of nonrenal mechanisms in chronic blood pressure control. This article explains the renal basis for the blood pressure set point by focusing on the absolute dependence of our survival on the maintenance of sodium balance. Two principal threats to sodium balance are discussed: (1) a change in sodium intake or renal excretory capability and (2) a change in blood pressure. In both instances, circulatory homeostasis is maintained because the sodium balance blood pressure set point is reached. © 2012 American Physiological Society. Compr Physiol 2:2481‐2494, 2012.

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Figure 1. Figure 1.

The direct effect of renal arterial pressure on sodium excretion in normal anesthetized dogs 29,30.
Figure 2. Figure 2.

Schematic of the renal‐body fluid feedback control system. Based on Guyton et al. 36.
Figure 3. Figure 3.

The acute pressure natriuresis effect in normal rats and rats infused with angiotensin II 82.
Figure 4. Figure 4.

Generation of the chronic renal function curve. The left panel shows how the blood pressure versus sodium excretion relationship is measured, by manipulating sodium intake and measuring steady‐state blood pressure. The right panel shows how those data typically are presented, to keep the axis consistent with those in the acute pressure natriuresis relationship.
Figure 5. Figure 5.

Sodium excretion and blood pressure responses to changes in sodium intake. The dotted line shows that sodium excretion normally rises rapidly to match an increase in sodium intake, such that blood pressure changes only minimally. However, the dashed line shows that when renal sodium excretory capability is impaired, sodium balance takes longer to achieve. The result is an increase in extracellular fluid volume and blood pressure.
Figure 6. Figure 6.

Relationships between mean arterial pressure and sodium excretion (as an index of sodium intake) after steady state was achieved at four levels of sodium intake in dogs 47. Sodium intakes ranging from approximately 5‐500 mEq/day were provided under normal conditions with a functional renin‐angiotensin system, after blockade of AngII formation with chronic angiotensin‐converting‐enzyme (ACE) inhibitor, and after infusing AngII continuously at 5 ng/kg/min to prevent plasma AngII levels from being suppressed on the high‐salt diet. Note the sensitivity of blood pressure to sodium intake when AngII levels are prevented from changing.
Figure 7. Figure 7.

The renal function curve in dogs with reduced kidney mass and placed on high‐salt diet (dashed line) 49. The solid line is the chronic renal function curve in the normal dogs from Figure 6. The decreased slope in the dogs with reduced kidney mass shows salt sensitivity of blood pressure (∼ 15 mmHg increase in arterial pressure).
Figure 8. Figure 8.

The renal function curves for the normal and AngII‐infused dogs in Figure 6 are redrawn in the left panel. The right panel shows predicted acute pressure natriuresis curves in normal versus AngII‐hypertensive animals. The arrow in the middle shows those acute curves being superimposed on the chronic curves, and the pair of curves at the top is meant to illustrate that the acute pressure natriuresis relationship can be measured under at any baseline sodium intake.
Figure 9. Figure 9.

The frequency distribution of blood pressure measurements throughout the day in chronically instrumented dogs under normal conditions or in dogs with sinoaortic denervation 13. Without baroreceptor function, blood pressure variability is increased markedly, but there is not a change in the blood pressure set point, that is, mean arterial pressure.
Figure 10. Figure 10.

Mean arterial pressure, cumulative sodium balance, and sodium excretion during chronic i.v. infusion of AngII at 5 ng/kg/min, but with an inflatable occluder on the renal artery to prevent the kidneys from experiencing the hypertension. Note that renal artery pressure was not decreased below normal, but was maintained at control levels by continuous servo‐controlled adjustment of the occluder. Sodium escape was prevented until the occluder was released. Redrawn, with permission, from data in Hall et al. 45.
Figure 11. Figure 11.

Chronic AngII infusion in normal mice (wild type), mice with knockout of the AT1A AngII receptor (Total KO), wild‐type mice that have kidneys transplanted from KO mice (Kidney KO), and KO mice that have kidneys transplanted from wild type mice (Systemic KO). MAP increased to the same level in wild‐type and systemic KO mice, showing that AngII hypertension only required renal AT1A receptors. Similarly, chronic AngII hypertension did not occur in mice with Total or Renal KO of AT1A receptors 17.


Figure 1.

The direct effect of renal arterial pressure on sodium excretion in normal anesthetized dogs 29,30.



Figure 2.

Schematic of the renal‐body fluid feedback control system. Based on Guyton et al. 36.



Figure 3.

The acute pressure natriuresis effect in normal rats and rats infused with angiotensin II 82.



Figure 4.

Generation of the chronic renal function curve. The left panel shows how the blood pressure versus sodium excretion relationship is measured, by manipulating sodium intake and measuring steady‐state blood pressure. The right panel shows how those data typically are presented, to keep the axis consistent with those in the acute pressure natriuresis relationship.



Figure 5.

Sodium excretion and blood pressure responses to changes in sodium intake. The dotted line shows that sodium excretion normally rises rapidly to match an increase in sodium intake, such that blood pressure changes only minimally. However, the dashed line shows that when renal sodium excretory capability is impaired, sodium balance takes longer to achieve. The result is an increase in extracellular fluid volume and blood pressure.



Figure 6.

Relationships between mean arterial pressure and sodium excretion (as an index of sodium intake) after steady state was achieved at four levels of sodium intake in dogs 47. Sodium intakes ranging from approximately 5‐500 mEq/day were provided under normal conditions with a functional renin‐angiotensin system, after blockade of AngII formation with chronic angiotensin‐converting‐enzyme (ACE) inhibitor, and after infusing AngII continuously at 5 ng/kg/min to prevent plasma AngII levels from being suppressed on the high‐salt diet. Note the sensitivity of blood pressure to sodium intake when AngII levels are prevented from changing.



Figure 7.

The renal function curve in dogs with reduced kidney mass and placed on high‐salt diet (dashed line) 49. The solid line is the chronic renal function curve in the normal dogs from Figure 6. The decreased slope in the dogs with reduced kidney mass shows salt sensitivity of blood pressure (∼ 15 mmHg increase in arterial pressure).



Figure 8.

The renal function curves for the normal and AngII‐infused dogs in Figure 6 are redrawn in the left panel. The right panel shows predicted acute pressure natriuresis curves in normal versus AngII‐hypertensive animals. The arrow in the middle shows those acute curves being superimposed on the chronic curves, and the pair of curves at the top is meant to illustrate that the acute pressure natriuresis relationship can be measured under at any baseline sodium intake.



Figure 9.

The frequency distribution of blood pressure measurements throughout the day in chronically instrumented dogs under normal conditions or in dogs with sinoaortic denervation 13. Without baroreceptor function, blood pressure variability is increased markedly, but there is not a change in the blood pressure set point, that is, mean arterial pressure.



Figure 10.

Mean arterial pressure, cumulative sodium balance, and sodium excretion during chronic i.v. infusion of AngII at 5 ng/kg/min, but with an inflatable occluder on the renal artery to prevent the kidneys from experiencing the hypertension. Note that renal artery pressure was not decreased below normal, but was maintained at control levels by continuous servo‐controlled adjustment of the occluder. Sodium escape was prevented until the occluder was released. Redrawn, with permission, from data in Hall et al. 45.



Figure 11.

Chronic AngII infusion in normal mice (wild type), mice with knockout of the AT1A AngII receptor (Total KO), wild‐type mice that have kidneys transplanted from KO mice (Kidney KO), and KO mice that have kidneys transplanted from wild type mice (Systemic KO). MAP increased to the same level in wild‐type and systemic KO mice, showing that AngII hypertension only required renal AT1A receptors. Similarly, chronic AngII hypertension did not occur in mice with Total or Renal KO of AT1A receptors 17.

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Article Title: Chronic Blood Pressure Control
 

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Michael W. Brands. Chronic Blood Pressure Control. Compr Physiol 2012, 2: 2481-2494. doi: 10.1002/cphy.c100056