Endothelial-derived nitric oxide modulates increased arterial water permeability in heart failure following myocardial infarction in rats

C. A. Hoover, M. A. Gaballa, Steven Goldman

Research output: Contribution to journalArticle

Abstract

Background: Hydraulic conductivity (Lp) is a measurement of arter al water permeability and is determined by complex structural and functional interactions between extracellular matrix and endothelial and smooth muscle cells. Bulk transport of lipoproteins and other large molecules depends critically on Lp. Lp in large arteries is elevated in the rat myocardlal infarction (MI) model of heart failure (HF). This increase in Lp is normalized by treatment with captopnl. Nitric oxide (NO) release is impaired in HF, however, its role in regulating Lp in intact arteries is unknown. We examined the effect of acute inhibition of endothelium-dependent NO release on Lp in treated and untreated HF. Methods and Results: Rats underwent experimental MI or sham operations; both groups were randomly assigned to treatment with captopril (C, 2g/L drinking water) for three weeks. Lp was determined using an in situ preparation of the carotid artery at a perfusion pressure of 60 mm Hg with and without L-NAME to inhibit NO release. Sham (N=10) Sham/C (N=9) HF (N=6) HF/C (N=6) Lp Baseline 6.1±1.8 5.0±2.0 8.3±2.0 * 5.0±1.0 Lp L-NAME 6.6±2.5 5.2±1.8 4.8±1.0 1 7.8±1.5 ** * p<0.05 compared to Sham baseline; 1 p<0.003 compared to HF baseline; **p<0.005 compared to HF/C baseline. Conclusions: NO plays no role in the acute regulation of large artery Lp in normal animals. However, blockade of NO release in captopril-treated HF returns Lp towards untreated HF values, suggesting that captopril improves Lp by normalizing NO production or release. NO inhibition acutely reduces the increased in Lp seen in HF; the pathogenesis of these changes is unclear and merits further evaluation.

Original languageEnglish (US)
JournalJournal of Investigative Medicine
Volume44
Issue number1
StatePublished - 1996

Fingerprint

Rats
Permeability
Nitric Oxide
Heart Failure
Myocardial Infarction
Water
Captopril
Arteries
NG-Nitroarginine Methyl Ester
Infarction
Hydraulic conductivity
Carotid Arteries
Drinking Water
Lipoproteins
Smooth Muscle Myocytes
Endothelium
Extracellular Matrix
Muscle
Animals
Perfusion

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{2cd6f8907f764085a5af230ffd346ee9,
title = "Endothelial-derived nitric oxide modulates increased arterial water permeability in heart failure following myocardial infarction in rats",
abstract = "Background: Hydraulic conductivity (Lp) is a measurement of arter al water permeability and is determined by complex structural and functional interactions between extracellular matrix and endothelial and smooth muscle cells. Bulk transport of lipoproteins and other large molecules depends critically on Lp. Lp in large arteries is elevated in the rat myocardlal infarction (MI) model of heart failure (HF). This increase in Lp is normalized by treatment with captopnl. Nitric oxide (NO) release is impaired in HF, however, its role in regulating Lp in intact arteries is unknown. We examined the effect of acute inhibition of endothelium-dependent NO release on Lp in treated and untreated HF. Methods and Results: Rats underwent experimental MI or sham operations; both groups were randomly assigned to treatment with captopril (C, 2g/L drinking water) for three weeks. Lp was determined using an in situ preparation of the carotid artery at a perfusion pressure of 60 mm Hg with and without L-NAME to inhibit NO release. Sham (N=10) Sham/C (N=9) HF (N=6) HF/C (N=6) Lp Baseline 6.1±1.8 5.0±2.0 8.3±2.0 * 5.0±1.0 Lp L-NAME 6.6±2.5 5.2±1.8 4.8±1.0 1 7.8±1.5 ** * p<0.05 compared to Sham baseline; 1 p<0.003 compared to HF baseline; **p<0.005 compared to HF/C baseline. Conclusions: NO plays no role in the acute regulation of large artery Lp in normal animals. However, blockade of NO release in captopril-treated HF returns Lp towards untreated HF values, suggesting that captopril improves Lp by normalizing NO production or release. NO inhibition acutely reduces the increased in Lp seen in HF; the pathogenesis of these changes is unclear and merits further evaluation.",
author = "Hoover, {C. A.} and Gaballa, {M. A.} and Steven Goldman",
year = "1996",
language = "English (US)",
volume = "44",
journal = "Journal of Investigative Medicine",
issn = "1081-5589",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Endothelial-derived nitric oxide modulates increased arterial water permeability in heart failure following myocardial infarction in rats

AU - Hoover, C. A.

AU - Gaballa, M. A.

AU - Goldman, Steven

PY - 1996

Y1 - 1996

N2 - Background: Hydraulic conductivity (Lp) is a measurement of arter al water permeability and is determined by complex structural and functional interactions between extracellular matrix and endothelial and smooth muscle cells. Bulk transport of lipoproteins and other large molecules depends critically on Lp. Lp in large arteries is elevated in the rat myocardlal infarction (MI) model of heart failure (HF). This increase in Lp is normalized by treatment with captopnl. Nitric oxide (NO) release is impaired in HF, however, its role in regulating Lp in intact arteries is unknown. We examined the effect of acute inhibition of endothelium-dependent NO release on Lp in treated and untreated HF. Methods and Results: Rats underwent experimental MI or sham operations; both groups were randomly assigned to treatment with captopril (C, 2g/L drinking water) for three weeks. Lp was determined using an in situ preparation of the carotid artery at a perfusion pressure of 60 mm Hg with and without L-NAME to inhibit NO release. Sham (N=10) Sham/C (N=9) HF (N=6) HF/C (N=6) Lp Baseline 6.1±1.8 5.0±2.0 8.3±2.0 * 5.0±1.0 Lp L-NAME 6.6±2.5 5.2±1.8 4.8±1.0 1 7.8±1.5 ** * p<0.05 compared to Sham baseline; 1 p<0.003 compared to HF baseline; **p<0.005 compared to HF/C baseline. Conclusions: NO plays no role in the acute regulation of large artery Lp in normal animals. However, blockade of NO release in captopril-treated HF returns Lp towards untreated HF values, suggesting that captopril improves Lp by normalizing NO production or release. NO inhibition acutely reduces the increased in Lp seen in HF; the pathogenesis of these changes is unclear and merits further evaluation.

AB - Background: Hydraulic conductivity (Lp) is a measurement of arter al water permeability and is determined by complex structural and functional interactions between extracellular matrix and endothelial and smooth muscle cells. Bulk transport of lipoproteins and other large molecules depends critically on Lp. Lp in large arteries is elevated in the rat myocardlal infarction (MI) model of heart failure (HF). This increase in Lp is normalized by treatment with captopnl. Nitric oxide (NO) release is impaired in HF, however, its role in regulating Lp in intact arteries is unknown. We examined the effect of acute inhibition of endothelium-dependent NO release on Lp in treated and untreated HF. Methods and Results: Rats underwent experimental MI or sham operations; both groups were randomly assigned to treatment with captopril (C, 2g/L drinking water) for three weeks. Lp was determined using an in situ preparation of the carotid artery at a perfusion pressure of 60 mm Hg with and without L-NAME to inhibit NO release. Sham (N=10) Sham/C (N=9) HF (N=6) HF/C (N=6) Lp Baseline 6.1±1.8 5.0±2.0 8.3±2.0 * 5.0±1.0 Lp L-NAME 6.6±2.5 5.2±1.8 4.8±1.0 1 7.8±1.5 ** * p<0.05 compared to Sham baseline; 1 p<0.003 compared to HF baseline; **p<0.005 compared to HF/C baseline. Conclusions: NO plays no role in the acute regulation of large artery Lp in normal animals. However, blockade of NO release in captopril-treated HF returns Lp towards untreated HF values, suggesting that captopril improves Lp by normalizing NO production or release. NO inhibition acutely reduces the increased in Lp seen in HF; the pathogenesis of these changes is unclear and merits further evaluation.

UR - http://www.scopus.com/inward/record.url?scp=33749542785&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749542785&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:33749542785

VL - 44

JO - Journal of Investigative Medicine

JF - Journal of Investigative Medicine

SN - 1081-5589

IS - 1

ER -