Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Houston, D. S.; Shepherd, John T.; Vanhoutte, Paul M.

doi:10.1172/jci112606

Cited by 169 publications

(70 citation statements)

References 26 publications

(35 reference statements)

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“…34 - 35 In contrast, in arteries with denuded endothelium, platelets produce contraction that appears to be mediated by thromboxane and serotonin. 35 Several studies indicate that aggregation of platelets can reduce blood flow, 8 11 demonstrated a cyclic reduction in coronary blood flow in dogs caused by periodic formation of platelet aggregates at the site of endothehal injury followed by spontaneous dissolution.…”

Section: Mechanisms Of Altered Vascular Response To Activated Plateletsmentioning

confidence: 99%

Vascular responses to platelet activation in normal and atherosclerotic primates in vivo.

Kaul

Heistad

Mügge

et al. 1991

Arterioscler Thromb

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Platelets release vasoactive substances that may contribute to augmented vasoconstriction. In this study, we examined vascular responses to activation of platelets in vivo by infusion of collagen. Purified bovine collagen was infused into the blood-perfused hind limb of normal and atherosclerotic cynomolgus monkeys. Resistance of the total limb and large arteries was measured at constant flow. In normal monkeys, collagen produced a decrease in total limb resistance, with a modest constrictor response of the large arteries. In atherosclerotic monkeys, collagen produced a transient, small decrease in total limb resistance, with pronounced constriction of large arteries. Indomethacin (5 mg/kg i.v.) and the thromboxane Aj/prostaglandin H 2 receptor antagonist SQ29,548 (2 mg/kg i.v.) virtually abolished the large-artery constrictor response to collagen in atherosclerotic monkeys. The 5-HT 2 -serotonergic receptor antagonist ketanserin (0.6 mg/kg i.v.) had no effect on the vasoconstrictor response. We conclude that 1) large arteries constrict and small vessels dilate in response to collagenmediated activation of platelets in vivo in normal and atherosclerotic monkeys, 2) large-artery constriction in response to activation of platelets is augmented in atherosclerotic monkeys, and 3) the augmented large-artery constriction in atherosclerotic monkeys may be mediated primarily by thromboxane. The findings provide evidence that platelets may contribute to augmented constrictor responses of atherosclerotic arteries. (Arteriosclerosis and Thrombosis 1991;11:1745-1751)

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Section: Mechanisms Of Altered Vascular Response To Activated Plateletsmentioning

confidence: 99%

Vascular responses to platelet activation in normal and atherosclerotic primates in vivo.

Kaul

Heistad

Mügge

et al. 1991

Arterioscler Thromb

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“…Inhibition of thromboxane A 2 production using a thromboxane synthase blocker (dazoxiben) or a thromboxane A 2 receptor antagonist (SQ29,548) attenuated contraction of the denuded coronary artery rings in response to aggregating platelets. 12 These results indicate that thromboxane A 2 is an important mediator of plateletinduced coronary artery constriction, whereas an intact endothelium is necessary for the relaxation of coronary artery segments in response to platelet aggregation. The purpose of this study was to determine the effects of intravascular platelet activation on coronary collateral blood flow by measuring the response to PAF in an in vivo canine model.…”

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confidence: 78%

“…Infusion of PAF into the normal coronary circulation typically yields a biphasic response, with initial vasodilation followed by vasoconstriction. 9 -11 Houston et al 12 observed that exposure of isolated coronary artery rings to aggregating platelets resulted in relaxation, but after removal of the endothelium, exposure to aggregating platelets caused contraction. Inhibition of thromboxane A 2 production using a thromboxane synthase blocker (dazoxiben) or a thromboxane A 2 receptor antagonist (SQ29,548) attenuated contraction of the denuded coronary artery rings in response to aggregating platelets.…”

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confidence: 99%

“…7 Aggregating platelets release multiple vasoactive substances, including thromboxane A 2 , serotonin, ADP, and histamine. 8,12 Houston et al 12 demonstrated that aggregating platelets caused relaxation of preconstricted coronary artery rings. This was an endothelium-dependent response, because aggregating platelets resulted in vasoconstriction of denuded coronary artery rings that could be blocked with selective antagonists of thromboxane A 2 and serotonin.…”

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confidence: 99%

“…13,29 -31 Furthermore, although it is unknown whether SQ30,741 directly affects PAF-induced platelet aggregation, the thromboxane A 2 receptor antagonist SQ29,548 does not inhibit platelet aggregation in response to ADP in vitro. 12 In addition, Aprill et al 15 found that pretreatment with the thromboxane synthase inhibitor UK38,485 abolished the increase of measured thromboxane B 2 generated in response to PAF but did not alter PAF-induced platelet aggregation. Therefore, it is unlikely that blockade of PAF-induced collateral constriction by SQ30,741 in the present study resulted from inhibition of PAF-induced platelet aggregation.…”

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confidence: 99%

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Effect of Platelet Activation on Coronary Collateral Blood Flow

Kinn

Bache

1998

Circulation

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Background-The platelet products thromboxane A 2 and serotonin have been shown to cause constriction of welldeveloped coronary collateral vessels. This study was performed to determine whether intravascular platelet activation produced with platelet activating factor (PAF) can cause a decrease in coronary collateral blood flow. Methods and Results-Collateral vessel growth was induced by embolization of a hollow stainless steel plug into the left anterior descending coronary artery (LAD) of adult dogs. The animals were returned to the laboratory 3 to 6 weeks later for surgical instrumentation and measurement of collateral blood flow. Collateral flow was assessed by measuring retrograde blood flow from the cannulated collateral-dependent artery. PAF (10 nmol) was injected into the left main coronary artery to allow products of platelet activation to reach collateral vessels arising from the left coronary system. PAF caused a vasoconstrictor response, which became maximal 3 minutes after injection and resulted in a 40.3Ϯ7.4% decrease in retrograde blood flow (32.1Ϯ2.1 to 19.6Ϯ3.2 mL/min; PϽ0.05). By 15 minutes after the PAF injection, both retrograde blood flow and transcollateral resistance had returned to normal. After pretreatment with the thromboxane A 2 receptor antagonist SQ30,741, the vasoconstrictor response to PAF was abolished and, in contrast to the decrease in retrograde blood flow from PAF alone, a weak vasodilator effect was unmasked. Conclusions-PAF caused a decrease in coronary collateral blood flow. This vasoconstrictor response required the participation of thromboxane A 2 .

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Effects of platelets on the protein expression in aortic segments: A proteomic approach

Modrego

Moñux

Mateos-Cáceres

et al. 2010

J of Cellular Biochemistry

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It is well known the effects of the vascular wall on platelet activity but little is known about the effects of platelets on the proteins expression in the vascular wall. We analyzed whether platelets may modify the protein expression in the vascular wall. We used an in vitro model coincubating human platelet rich plasma (PRP) with control and 10 ng/ml tumor necrosis factor-α (TNF-α)-preincubated bovine aortic segments. 2DE, mass spectrometry and Western blot analysis were used to determine changes in the expression of proteins associated with the cytoskeleton and energetic metabolism in the aortic segments. In control healthy vascular wall, only the cytoskeleton-related proteins expression was modified by PRP. However, when PRP was coincubated with TNF-α pre-stimulated aortic segments lesser number of cytoskeleton-related proteins were modified. With respect to energetic metabolism, in control segments, PRP failed to modify any of the analyzed energetic-related proteins. However, in TNF-α-preincubated segments the presence of PRP upexpressed glyceraldehyde-3-phosphate dehydrogenase. Moreover, by western blot experiments it was observed that in TNF-α-preincubated segments the expression of fructose 1,6-bisphosphate aldolase was downregulated by platelets. However, no differences were found in the expression of triosephosphate isomerase and ATP synthase α-chain. In addition, the activity of fructose 1,6-bisphosphate aldolase and piruvate content was significantly reduced without modification on triosephosphate isomerase activity. In conclusion, the crosstalk between platelets and vascular wall is bidirectional and platelets regulated in the vascular wall the expression of proteins associated with the cytoskeleton and energetic metabolism, particularly in the healthy vascular wall.

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Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Cited by 169 publications

References 26 publications

Vascular responses to platelet activation in normal and atherosclerotic primates in vivo.

Vascular responses to platelet activation in normal and atherosclerotic primates in vivo.

Effect of Platelet Activation on Coronary Collateral Blood Flow

Effects of platelets on the protein expression in aortic segments: A proteomic approach

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