Abstract
A number of naturally occurring substances can evoke endothelium-dependent responses in isolated blood vessels. In most arteries studied, acetylcholine, adenosine diphosphate (ADP), adenosine triphosphate (ATP), arachidonic acid, bradykinin, and thrombin cause endothelium-dependent relaxations. In veins, however, the endothelium-dependent inhibitory effect of acetylcholine, ATP, and thrombin often is transient and/or modest, as it is masked by the direct stimulating action of these substances on the venous smooth muscle; arachidonic acid evokes endothelium-dependent augmentation of the contractile response to norepinephrine. Aggregating platelets cause an endothelium-dependent relaxation of certain but not all arteries and veins that is probably me-diated by released serotonin and ADP. The endothelium of the coronary artery may enhance the relaxations caused by catecholamines. Vasopressin causes endothelium-dependent relaxations in cerebral and coronary arteries but not in systemic blood vessels. Hypoxia causes endothelium-dependent increases in tension in systemic arteries and in pulmonary arteries and veins but not in limb veins. The heterogeneity in endothelium-dependent responsiveness may reflect variations in sensitivity of either endothelial or vascular smooth-muscle cells of different anatomical origin.
Original language | English (US) |
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Pages (from-to) | S12-S23 |
Journal | Journal of Cardiovascular Pharmacology |
Volume | 7 |
DOIs | |
State | Published - 1985 |
Keywords
- Acetylcholine
- Adenosine nucleotides
- Aggregating platelets
- Arachidonic acid
- Arteries
- Endothelium
- Serotonin
- Thrombin
- Vascular smooth muscle
- Veins
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine