Interactions between angiotensin II and the sympathetic nervous system in the long-term control of arterial pressure

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Abstract

The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.

Original languageEnglish (US)
Pages (from-to)83-90
Number of pages8
JournalClinical and Experimental Pharmacology and Physiology
Volume24
Issue number1
StatePublished - 1997

Fingerprint

Sympathetic Nervous System
Angiotensin II
Arterial Pressure
Sodium
Hypertension
Baroreflex
Extracellular Fluid
Renin-Angiotensin System
Blood Volume
Salts
Blood Pressure
Pressure

Keywords

  • blood pressure
  • Dahl salt-sensitive rat
  • reduced renal mass hypertension
  • renin-angiotensin system
  • salt-sensitive hypertension
  • sympathetic nervous system

ASJC Scopus subject areas

  • Physiology
  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

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title = "Interactions between angiotensin II and the sympathetic nervous system in the long-term control of arterial pressure",
abstract = "The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.",
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N2 - The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.

AB - The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.

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