Angiotensin II, nitric oxide, and end-organ damage in hypertension

A. Bataineh, Leopoldo Raij

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

The adaptive changes that accompany hypertension and involve the kidney, heart, and vessels, namely, muscle hypertrophy/hyperplasia, endothelial dysfunction and extracellular matrix increase can, in fact, be maladaptive and eventually lead to end-organ disease, such as renal failure, heart failure, and coronary disease. However, these changes. vary markedly between individuals with similar levels of hypertension. Nitric oxide (NO), an endogenous vasodilator and inhibitor of vascular smooth muscle and mesangial cell growth, is synthesized in the endothelium by a constitutive NO synthase (NOS). NO antagonizes the effects of angiotensin II on vascular tone and growth and also downregulates the synthesis of angiotensin converting enzyme (ACE) and angiotensin II type 1 (AT-1) receptors. In hypertension, the physiologic response to the increased shear stress and cyclic strain is to upregulate NOS activity in endothelial cells. Upregulation of vascular NOS activity is a homeostatic adaptation to the increased hemodynamic workload that may help in preventing end-organ damage. Indeed, hypertension-prone salt-sensitive rats manifest a decrease (instead of an increase) in vascular NOS activity when hypertensive; these rats develop severe vascular hypertrophy, left ventricular hypertrophy, and renal injury. Studies in hypertensive humans suggest that, independent of the effects of salt on blood pressure, salt sensitivity may be a marker for susceptibility to the development of endothelial dysfunction as well as cardiovascular and renal injury. We hypothesize that in hypertension, recognition of markers of cardiovascular susceptibility to injury and the understanding of the pathophysiological mechanisms involved may open new opportunities for therapeutic intervention. In this context, only those antihypertensive agents that lower blood pressure and concomitantly restore the homeostatic balance of vasoactive agents such as angiotensin II and NO within the vessel wall would be effective in preventing or arresting end-organ disease.

Original languageEnglish
JournalKidney International, Supplement
Volume54
Issue number68
StatePublished - Jan 1 1998
Externally publishedYes

Fingerprint

Angiotensin II
Nitric Oxide
Nitric Oxide Synthase
Blood Vessels
Hypertension
Salts
Kidney
Hypertrophy
Wounds and Injuries
Up-Regulation
Blood Pressure
Angiotensin Type 1 Receptor
Mesangial Cells
Left Ventricular Hypertrophy
Peptidyl-Dipeptidase A
Growth
Workload
Vasodilator Agents
Vascular Smooth Muscle
Antihypertensive Agents

Keywords

  • Angiotensin II
  • Hypertension
  • Left ventricular hypertrophy
  • Nitric oxide
  • Renal injury

ASJC Scopus subject areas

  • Nephrology

Cite this

Angiotensin II, nitric oxide, and end-organ damage in hypertension. / Bataineh, A.; Raij, Leopoldo.

In: Kidney International, Supplement, Vol. 54, No. 68, 01.01.1998.

Research output: Contribution to journalArticle

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