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 language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)