Hypertension and cardiovascular risk factors role of the angiotensin ii-nitric oxide interaction

Leopoldo Raij

Research output: Contribution to journalArticle

93 Citations (Scopus)

Abstract

Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain-all the vascular pathophysiology of hypertension, but it certainly appears to be an important component. In hypertension, salt sensitivity, whether primmary (ie, certain populations in the United States and Japan) or secondary (ie, aging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.

Original languageEnglish
Pages (from-to)767-773
Number of pages7
JournalHypertension
Volume37
Issue number2 II
StatePublished - Mar 19 2001
Externally publishedYes

Fingerprint

Angiotensins
Nitric Oxide
Hypertension
Angiotensin II
Blood Vessels
Kidney
Workload
Type 2 Diabetes Mellitus
Atherosclerosis
Japan
Up-Regulation
Salts
Hemodynamics
Blood Pressure
Morbidity
Mortality
Population

Keywords

  • Angiotensin II
  • Endothelium
  • Nitric oxide
  • Stress

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Hypertension and cardiovascular risk factors role of the angiotensin ii-nitric oxide interaction. / Raij, Leopoldo.

In: Hypertension, Vol. 37, No. 2 II, 19.03.2001, p. 767-773.

Research output: Contribution to journalArticle

@article{5fd6660b28ea49c9a08cba448df1717b,
title = "Hypertension and cardiovascular risk factors role of the angiotensin ii-nitric oxide interaction",
abstract = "Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain-all the vascular pathophysiology of hypertension, but it certainly appears to be an important component. In hypertension, salt sensitivity, whether primmary (ie, certain populations in the United States and Japan) or secondary (ie, aging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.",
keywords = "Angiotensin II, Endothelium, Nitric oxide, Stress",
author = "Leopoldo Raij",
year = "2001",
month = "3",
day = "19",
language = "English",
volume = "37",
pages = "767--773",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "2 II",

}

TY - JOUR

T1 - Hypertension and cardiovascular risk factors role of the angiotensin ii-nitric oxide interaction

AU - Raij, Leopoldo

PY - 2001/3/19

Y1 - 2001/3/19

N2 - Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain-all the vascular pathophysiology of hypertension, but it certainly appears to be an important component. In hypertension, salt sensitivity, whether primmary (ie, certain populations in the United States and Japan) or secondary (ie, aging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.

AB - Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain-all the vascular pathophysiology of hypertension, but it certainly appears to be an important component. In hypertension, salt sensitivity, whether primmary (ie, certain populations in the United States and Japan) or secondary (ie, aging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.

KW - Angiotensin II

KW - Endothelium

KW - Nitric oxide

KW - Stress

UR - http://www.scopus.com/inward/record.url?scp=0035096830&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035096830&partnerID=8YFLogxK

M3 - Article

VL - 37

SP - 767

EP - 773

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 2 II

ER -