Temperature-dependent basal tone in isolated human saphenous veins: implication of TP-receptors.
Cutaneous blood vessels are very sensitive to changes in environmental temperature. The influence of variations in local temperature on the mechanisms involved in the basal tone, present in isolated human saphenous veins has not yet been studied. In the present study, segments with and without endothelium of human saphenous veins obtained from coronary bypass surgery patients were mounted for isometric tension recording in oxygenated physiological salt solution (PSS). After stabilisation of the basal tone, the local temperature was rapidly either decreased from 37 degrees C to 24 degrees C (cooling) or increased from 37 degrees C to 42 degrees C (warming). When antagonists or inhibitors were used the preparations were incubated for 30 min with the drugs. During basal conditions, cooling caused relaxations of the saphenous vein segments with endothelium and warming caused contractions; the absence of the endothelium did not modify these responses. In veins without endothelium, the warming-induced contractions were significantly inhibited by verapamil (10 microM) and by the antagonist of TP-receptors (receptors for thromboxane A2) Bay u 3405 (1 microM). The warming induced contractions were not affected by cyclooxygenase or lipoxygenase inhibition. At 37 degrees C, the isoprostanes (8-iso-PGE2 and 8-iso-PGF2alpha) induced potent contractions that were significantly inhibited by Bay u 3405 (1 microM). The data show that a basal tone is present in isolated resting human saphenous vein segments at 37 degrees C. This basal tone is decreased by local cooling and enhanced by local warming and is not dependent on the presence of the endothelium. The warming-induced contraction of the veins is mediated by a non-cyclooxygenase, non-lipoxygenase metabolite (isoprostane?) that interacts with TP-receptors and via an extracellular calcium-dependent pathway.
Simonet
S
S
Division of Angiology, Institut de Recherches Servier, Suresnes, France.
Bonhomme
E
E
Fabiani
J N
JN
Verbeuren
T
T
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002227:Carbazoles / Q000494:pharmacology; D015237:Dinoprost / Q000031:analogs & derivatives / Q000494:pharmacology; D004347:Drug Interactions; D016232:Endothelins / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism; D028441:F2-Isoprostanes; D006801:Humans; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D010646:Phentolamine / Q000494:pharmacology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D017482:Receptors, Thromboxane / Q000502:physiology*; D012501:Saphenous Vein / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D013449:Sulfonamides / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects; D013696:Temperature; D013928:Thromboxane A2 / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000378:metabolism / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D002227:Carbazoles; D016232:Endothelins; D028441:F2-Isoprostanes; D010975:Platelet Aggregation Inhibitors; D017482:Receptors, Thromboxane; D013449:Sulfonamides; D014662:Vasoconstrictor Agents; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D013928:Thromboxane A2; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D015237:Dinoprost; D011464:Epoprostenol; C063119:ramatroban; D002118:Calcium; D009638:Norepinephrine; D010646:Phentolamine