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

1987 ◽  
Author(s):  
W J Janssens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Pulmonary Arteries ◽  
Thromboxane A2 ◽  
Isometric Tension ◽  
Vasoconstrictor Effect ◽  
Smooth Muscle Contractions ◽  
Rat Platelets ◽  
Stimulation Of

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.

Effect of changes in pH on wall tension in isolated rat pulmonary artery: role of the RhoA/Rho-kinase pathway

2004 ◽  
Vol 287 (4) ◽  
pp. L673-L684 ◽  
Author(s):  
Jean-Marc Hyvelin ◽  
Clare O’Connor ◽  
Paul McLoughlin
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Kinase Inhibitor ◽  
Pulmonary Arteries ◽  
Rho Kinase ◽  
Systemic Circulation ◽  
Pulmonary Vasculature ◽  
Tension Development ◽  
Kinase Pathway

Pulmonary arteries (PA) are resistant to the vasodilator effects of extracellular acidosis in systemic vessels; the mechanism underlying this difference between systemic and pulmonary circulations has not been elucidated. We hypothesized that RhoA/Rho-kinase-mediated Ca2+ sensitization pathway played a greater role in tension development in pulmonary than in systemic vascular smooth muscle and that this pathway was insensitive to acidosis. In arterial rings contracted with the α1-agonist phenylephrine (PE), the Rho-kinase inhibitor Y-27632 (≤3 μM) induced greater relaxation in precontracted PA rings than in aortic rings. In PA rings stimulated by PE, the activation of RhoA was greater than in aorta. Normocapnic acidosis (NA) induced a smaller relaxation in precontracted PA than in aorta. However, in the presence of nifedipine and thapsigargin, when PE-induced contraction was predominantly mediated by Rho-kinase, the relaxant effect of NA was reduced and similar in both vessel types. Furthermore, in the presence of Y-27632, NA induced a greater relaxation in both PA and aorta, which was similar in both vessels. Finally, in α-toxin-permeabilized smooth muscle, PE-induced contraction at constant Ca2+ activity was inhibited by Y-27632 and unaffected by acidosis. These results indicate that Ca2+ sensitization induced by the RhoA/Rho-kinase pathway played a greater role in agonist-induced vascular smooth muscle contraction in PA than in aorta and that tension mediated by this pathway was insensitive to acidosis. The predominant role of the RhoA/Rho-kinase pathway in the pulmonary vasculature may account for the resistance of this circulation to the vasodilator effect of acidosis observed in the systemic circulation.

Role of Ca2+ in vascular smooth muscle contractions induced by Phoneutria nigriventer spider venom

Toxicon ◽  
2004 ◽  
Vol 43 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Cleber E Teixeira ◽  
Alexandre P Corrado ◽  
Gilberto De Nucci ◽  
Edson Antunes
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Contractions ◽  
Spider Venom ◽  
Smooth Muscle Contractions ◽  
Phoneutria Nigriventer

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

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