VASOCONSTRICTOR EFFECTS OF AGGREGATING PLATELETS IN RABBIT PULMONARY ARTERIES WITH AND WITHOUT ENDOTHELIUM

Publisher Website
Google Scholar
Abstract
The aim of the present experiments was to investigate the modulatory role of the endothelium on vasoconstrictions induced by aggregating platelets. Rings of rabbit pulmonary arteries were mounted for isometric tension recording. The presence or absence of the endothelium was confirmed using acetylcholine-induced relaxations. All contractions were expressed as percentage of a K+-induced (100 mM) contraction. Thrombin was administered to the preparations at 0.5 NIH units/ml. At this concentration the enzyme caused no or only very small contractions, but apparently induced maximal platelet activation in this experimental setting. Cumulative administration of rat platelets in the presence of thrombin caused contractions of the arteries. These contractions occurred at lower platelet amounts and were larger in endothelium-deprived rings than in preparations with intact endothelium. This indicates that mediators released from aggregating platelets cause contraction of the vascular smooth muscle cells which are attenuated by (a) factor(s) released from the endothelium. Platelet-induced contractions were dose-dependently inhibited and finally abolished by the S2-serotonergic antagonist ketanserin and inhibited to a lesser extent by the thromboxane A2 antagonist BM-13177. This indicates that serotonin, and to a lesser extent thromboxane A2, are the mediators of platelet-induced contractions and that mutual amplification of their vasoconstrictor effect may occur. Serotonin-induced contractions of pulmonary artery rings occurred at lower concentrations and were larger in endothelium-deprived preparations indicating that the endothelium derived factor(s) attenuating platelet-induced contraction may be released upon stimulation of the endothelium by serotonin. The pA2-value of ketanserin against serotonin-induced contractions was similar in endothelium-deprived preparations and preparations with intact endothelium. This indicates that the stimulating effect of serotonin on the endothelium is not mediated by the S2-serotonergic mechanism responsible for vascular smooth muscle contractions.

This publication has 0 references indexed in Scilit: