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.

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.

A P-Selectin/CD62P Monoclonal Antibody (LYP-20), in Tandem with Flow Cytometry, Detects in vivo Activated Circulating Rat Platelets in Severe Vascular Trauma

1994 ◽  
Vol 72 (05) ◽  
pp. 745-749 ◽  
Author(s):  
Elza Chignier ◽  
Maud Parise ◽  
Lilian McGregor ◽  
Caroline Delabre ◽  
Sylvie Faucompret ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Platelet Activation ◽  
Peripheral Blood ◽  
Vascular Trauma ◽  
Activated Platelets ◽  
Group I ◽  
Group Ii ◽  
Rat Platelets

SummaryP-selectin, also known as CD62P, GMP140 or PADGEM, is present in platelet a-granules and endothelial cell Weibel-Palade bodies and is very rapidly expressed on the surface of these cells on activation. In this study, an anti P-selectin monoclonal antibody (LYP20) was used, in tandem with flow cytometry, to identify activated platelets at the site of induced vascular trauma or in peripheral blood. Moreover, electron microscopy was performed to characterize sites of vascular trauma and quantify the number of adhering platelets. The same induced vascular trauma was observed to result into animals responding in 2 different ways (Group I, Group II) following the degree of platelet activation. Five rats, out of 14 with induced vascular trauma, had more than half of their circulating platelets expressing P-selectin when drawn at the site of the trauma (67.4% ± 3.44) or in peripheral blood (78.5% ± 2.5) (Group I). In the remaining 9 animals a much smaller proportion of circulating platelets expressed P-selectin when assayed from trauma sites (18% ± 3.34) or in peripheral blood (18.0% ± 4.30) (Group II). Enhanced P-selectin expression by circulating platelets in Group I, compared to Group II, appears to be linked to the degree of activated platelets adhering at sites of trauma (171 ± 15 × 103 platelets versus 48 ± 31 × 103 platelets per mm2). In the 5 control animals, that were not operated on, platelets expressing P-selectin when drawn at the site of a mock trauma (7.0% ± 1.84) or in the peripheral blood (11.2% ± 3.30) showed little activation. In addition, no platelet adhesion was seen on the vascular bed of these animals. Results from this study show that analysis of P-selectin (CD62P) expression, in circulating platelets, is a valuable and rapid marker of platelet activation following severe vascular trauma induced in rats. However, activated platelets were not detected to the same extent in the peripheral blood of all animals having undergone vascular trauma. It is conceivable that platelets, depending on the degree of activation, may be actively sequestered in organs and prevented from circulating. Alternatively, P-selectin may be rapidly endocytosed, or not expressed, by activated circulating platelets depending on the type of agonists implicated in vivo activation.

Effects of levobupivacaine on isolated rat tracheal smooth muscle

2015 ◽  
Vol 29 (5) ◽  
pp. 809-812 ◽  
Author(s):  
Hung-Chi Chang ◽  
Shin-Yan Chen ◽  
Yu-Feng Huang ◽  
Feng-Lin Liu ◽  
Yih-Giun Cherng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Tracheal Smooth Muscle ◽  
Rat Tracheal Smooth Muscle ◽  
Isolated Rat

Role of Cl− currents in rat aortic smooth muscle activation by prostaglandin F2α

2003 ◽  
Vol 481 (2-3) ◽  
pp. 133-140 ◽  
Author(s):  
Jihua Jiang ◽  
Peter H Backx ◽  
Hwee Teoh ◽  
Michael E Ward
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Prostaglandin F2α ◽  
Aortic Smooth Muscle

Levobupivacaine-induced contraction of isolated rat aorta is calcium dependent

2011 ◽  
Vol 89 (7) ◽  
pp. 467-476 ◽  
Author(s):  
Ji Seok Baik ◽  
Ju-Tae Sohn ◽  
Seong-Ho Ok ◽  
Jae-Gak Kim ◽  
Hui-Jin Sung ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Calcium Influx ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Guanosine Monophosphate ◽  
Response Curves ◽  
Calcium Dependent ◽  
Isolated Rat

Levobupivacaine is a long-acting local anesthetic that intrinsically produces vasoconstriction in isolated vessels. The goals of this study were to investigate the calcium-dependent mechanism underlying levobupivacaine-induced contraction of isolated rat aorta in vitro and to elucidate the pathway responsible for the endothelium-dependent attenuation of levobupivacaine-induced contraction. Isolated rat aortic rings were suspended to record isometric tension. Cumulative levobupivacaine concentration–response curves were generated in either the presence or absence of the antagonists verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, Gd3+, NW-nitro-l-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and methylene blue, either alone or in combination. Verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, low calcium concentrations, and calcium-free Krebs solution attenuated levobupivacaine-induced contraction. Gd3+ had no effect on levobupivacaine-induced contraction. Levobupivacaine increased intracellular calcium levels in vascular smooth muscle cells. L-NAME, ODQ, and methylene blue increased levobupivacaine-induced contraction in endothelium-intact aorta. SKF-96365 attenuated calcium-induced contraction in a previously calcium-free isotonic depolarizing solution containing 100 mmol/L KCl. Levobupivacaine-induced contraction of rat aortic smooth muscle is mediated primarily by calcium influx from the extracellular space mainly via voltage-operated calcium channels and, in part, by inositol 1,4,5-trisphosphate receptor-mediated release of calcium from the sarcoplasmic reticulum. The nitric oxide – cyclic guanosine monophosphate pathway is involved in the endothelium-dependent attenuation of levobupivacaine-induced contraction.

MP31-10 ADDITIVE CONTRACTIONS BY THROMBOXANE A2 AND ENDOTHELIN-1 ARE STRONGER THAN NOREPINEPHRINE-INDUCED CONTRACTIONS IN HUMAN PROSTATE SMOOTH MUSCLE

2015 ◽  
Vol 193 (4S) ◽  
Author(s):  
Martin Hennenberg ◽  
Alice C. Acevedo ◽  
Alexander Tamalunas ◽  
Yiming Wang ◽  
Beata Rutz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Thromboxane A2 ◽  
Human Prostate ◽  
Endothelin 1
Sign in / Sign up

Export Citation Format

Share Document