Abstract
Experiments were designed to determine whether nitric oxide was the mediator of increased endothelium-dependent relaxations in veins proximal to an arteriovenous fistula. A fistula was prepared between femoral arteries and veins in dogs. After 6 wk, veins proximal to the fistula were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers. In some rings the endothelium was removed deliberately. N(G)- monomethyl-L-arginine (L-NMMA) caused contraction in three of six fistula- operated veins with and without endothelium. In rings contracted submaximally with prostaglandin F(2α), acetylcholine and the α2-adrenergic agonist UK- 14,304 caused endothelium-dependent, concentration-dependent relaxations that were greater in fistula compared with sham-operated veins. These relaxations were reduced by L-NMMA. Calcium ionophore A23187 caused comparable endothelium-dependent relaxations in fistula- and sham-operated veins that were unaffected by L-NMMA. There were no differences in either calcium- dependent or -independent activity of nitric oxide synthase isolated from fistula- and sham-operated veins. Positive staining for nitric oxide synthase was present in both the endothelium and media of fistula-operated veins. These results indicate that nitric oxide mediates increased endothelium dependent relaxations to acetylcholine and α2-adrenergic agonists in fistula-operated veins. Therefore, chronic increases in blood flow and oxygen tension modify selectively receptor-coupled production of nitric oxide in endothelium and smooth muscle of veins.
Original language | English (US) |
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Pages (from-to) | H668-H673 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 271 |
Issue number | 2 40-2 |
DOIs | |
State | Published - Aug 1996 |
Keywords
- N(G)monomethyl-L-arginine
- arteriovenous fistula
- blood flow
- nitric oxide synthase
- shear stress
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)