El óxido nítrico en la hipertensión

Relación con el daño renal y la hipertrofia ventricular izquierda

Translated title of the contribution: Nitric oxid in hypertension: Relation with renal injury and left ventricular hypertrophy

Leopoldo Raij

Research output: Contribution to journalArticle

Abstract

Hypertension is accompanied by architectual changes in the kidney, heart, and vessels that are often maladaptive and can eventually contribute to end-organ disease such as renal failure, heart failure, and coronary disease. Nitric oxide, an endogenous vasodilator and antithrombotic agent synthesized in the endothelium by a constitutive nitric oxide synthase, inhibits growth-related responses to injury in vascular cells. Specifically, in the presence of hypertension, nitric oxide may work in the kidney by inhibiting both mesangial cell hypertrophy and hyperplasia as well as synthesis of extracellular matrix and in the heart and systemic vessels by modulating smooth muscle cell hypertrophy and hyperplasia. The effects of nitric oxide are antagonistic of the effects of angiotensin II. Sheart stress and cyclic strain, physical forces known to operate in hypertension, are accompanied by increases in endothelial nitric oxide synthase expression, nitric oxide synthase protein, and nitric oxide synthase activity in endothelial cells. Experimental studies using genetic models of hypertension show a variation in hypertension-modulated vascular nitric oxide synthase activity in different strains of rats. These studies suggest that upregulation of vascular nitric oxide synthase activity is a homeostatic adaptation to increased hemodynamic workload in hypertension and that this may help prevent end-organ damage. If these findings apply to humans, differences in end-organ disease seen in patients with similar degrees of hypertension may be due in part to genetic differences in vascular nitric oxide synthase activity in response to hypertension.

Original languageSpanish
Pages (from-to)12-17
Number of pages6
JournalRevista Espanola de Cardiologia
Volume52
Issue numberSUPPL. 3
StatePublished - Dec 1 1999
Externally publishedYes

Fingerprint

Left Ventricular Hypertrophy
Nitric Oxide Synthase
Hypertension
Kidney
Wounds and Injuries
Blood Vessels
Nitric Oxide
Hypertrophy
Hyperplasia
Mesangial Cells
Fibrinolytic Agents
Nitric Oxide Synthase Type III
Vascular System Injuries
Genetic Models
Workload
Vasodilator Agents
Angiotensin II
Smooth Muscle Myocytes
Endothelium
Renal Insufficiency

Keywords

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

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

El óxido nítrico en la hipertensión : Relación con el daño renal y la hipertrofia ventricular izquierda. / Raij, Leopoldo.

In: Revista Espanola de Cardiologia, Vol. 52, No. SUPPL. 3, 01.12.1999, p. 12-17.

Research output: Contribution to journalArticle

@article{f11ec4d2e33540eeb1b45a07e99e7028,
title = "El {\'o}xido n{\'i}trico en la hipertensi{\'o}n: Relaci{\'o}n con el da{\~n}o renal y la hipertrofia ventricular izquierda",
abstract = "Hypertension is accompanied by architectual changes in the kidney, heart, and vessels that are often maladaptive and can eventually contribute to end-organ disease such as renal failure, heart failure, and coronary disease. Nitric oxide, an endogenous vasodilator and antithrombotic agent synthesized in the endothelium by a constitutive nitric oxide synthase, inhibits growth-related responses to injury in vascular cells. Specifically, in the presence of hypertension, nitric oxide may work in the kidney by inhibiting both mesangial cell hypertrophy and hyperplasia as well as synthesis of extracellular matrix and in the heart and systemic vessels by modulating smooth muscle cell hypertrophy and hyperplasia. The effects of nitric oxide are antagonistic of the effects of angiotensin II. Sheart stress and cyclic strain, physical forces known to operate in hypertension, are accompanied by increases in endothelial nitric oxide synthase expression, nitric oxide synthase protein, and nitric oxide synthase activity in endothelial cells. Experimental studies using genetic models of hypertension show a variation in hypertension-modulated vascular nitric oxide synthase activity in different strains of rats. These studies suggest that upregulation of vascular nitric oxide synthase activity is a homeostatic adaptation to increased hemodynamic workload in hypertension and that this may help prevent end-organ damage. If these findings apply to humans, differences in end-organ disease seen in patients with similar degrees of hypertension may be due in part to genetic differences in vascular nitric oxide synthase activity in response to hypertension.",
keywords = "Angiotensin II, Hypertension, Left ventricular hypertrophy, Nitric oxide, Renal injury",
author = "Leopoldo Raij",
year = "1999",
month = "12",
day = "1",
language = "Spanish",
volume = "52",
pages = "12--17",
journal = "Revista Espanola de Cardiologia",
issn = "0300-8932",
publisher = "Ediciones Doyma, S.L.",
number = "SUPPL. 3",

}

TY - JOUR

T1 - El óxido nítrico en la hipertensión

T2 - Relación con el daño renal y la hipertrofia ventricular izquierda

AU - Raij, Leopoldo

PY - 1999/12/1

Y1 - 1999/12/1

N2 - Hypertension is accompanied by architectual changes in the kidney, heart, and vessels that are often maladaptive and can eventually contribute to end-organ disease such as renal failure, heart failure, and coronary disease. Nitric oxide, an endogenous vasodilator and antithrombotic agent synthesized in the endothelium by a constitutive nitric oxide synthase, inhibits growth-related responses to injury in vascular cells. Specifically, in the presence of hypertension, nitric oxide may work in the kidney by inhibiting both mesangial cell hypertrophy and hyperplasia as well as synthesis of extracellular matrix and in the heart and systemic vessels by modulating smooth muscle cell hypertrophy and hyperplasia. The effects of nitric oxide are antagonistic of the effects of angiotensin II. Sheart stress and cyclic strain, physical forces known to operate in hypertension, are accompanied by increases in endothelial nitric oxide synthase expression, nitric oxide synthase protein, and nitric oxide synthase activity in endothelial cells. Experimental studies using genetic models of hypertension show a variation in hypertension-modulated vascular nitric oxide synthase activity in different strains of rats. These studies suggest that upregulation of vascular nitric oxide synthase activity is a homeostatic adaptation to increased hemodynamic workload in hypertension and that this may help prevent end-organ damage. If these findings apply to humans, differences in end-organ disease seen in patients with similar degrees of hypertension may be due in part to genetic differences in vascular nitric oxide synthase activity in response to hypertension.

AB - Hypertension is accompanied by architectual changes in the kidney, heart, and vessels that are often maladaptive and can eventually contribute to end-organ disease such as renal failure, heart failure, and coronary disease. Nitric oxide, an endogenous vasodilator and antithrombotic agent synthesized in the endothelium by a constitutive nitric oxide synthase, inhibits growth-related responses to injury in vascular cells. Specifically, in the presence of hypertension, nitric oxide may work in the kidney by inhibiting both mesangial cell hypertrophy and hyperplasia as well as synthesis of extracellular matrix and in the heart and systemic vessels by modulating smooth muscle cell hypertrophy and hyperplasia. The effects of nitric oxide are antagonistic of the effects of angiotensin II. Sheart stress and cyclic strain, physical forces known to operate in hypertension, are accompanied by increases in endothelial nitric oxide synthase expression, nitric oxide synthase protein, and nitric oxide synthase activity in endothelial cells. Experimental studies using genetic models of hypertension show a variation in hypertension-modulated vascular nitric oxide synthase activity in different strains of rats. These studies suggest that upregulation of vascular nitric oxide synthase activity is a homeostatic adaptation to increased hemodynamic workload in hypertension and that this may help prevent end-organ damage. If these findings apply to humans, differences in end-organ disease seen in patients with similar degrees of hypertension may be due in part to genetic differences in vascular nitric oxide synthase activity in response to hypertension.

KW - Angiotensin II

KW - Hypertension

KW - Left ventricular hypertrophy

KW - Nitric oxide

KW - Renal injury

UR - http://www.scopus.com/inward/record.url?scp=6244288473&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=6244288473&partnerID=8YFLogxK

M3 - Article

VL - 52

SP - 12

EP - 17

JO - Revista Espanola de Cardiologia

JF - Revista Espanola de Cardiologia

SN - 0300-8932

IS - SUPPL. 3

ER -