Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Altura, Burton M.; Chand, N.

doi:10.1111/j.1476-5381.1981.tb08734.x

Cited by 9 publications

(1 citation statement)

References 27 publications

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“…Other products of platelet aggregation, including catecholamines or thromboxane A2, may produce pulmonary vascular contraction (28)(29)(30)(31). The failure of cyclooxygenase inhibitors to alter the contractile response to platelets indicates, however, that thromboxane A2 is not an essential mediator of plateletevoked contraction of the canine pulmonary artery.…”

Section: Discussionmentioning

confidence: 95%

Aggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine.

McGoon¹,

Vanhoutte²

1984

J. Clin. Invest.

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Abstract. To examine the effect of platelets and 5-hydroxytryptamine on pulmonary arterial smooth muscle, rings of canine pulmonary arteries, with and without endothelium, were studied under isometric conditions in physiological salt solution. 5-Hydroxytryptamine, but not the thromboxane-like endoperoxide analogue U-466 19, produced concentration-dependent contractions of the rings with a maximum averaging 93% of that obtained with KCL. Autologous platelets in concentrations comparable to that in plasma caused contractions averaging 70% of the maximal responses to KCL. Solution withdrawn from baths containing platelet-contracted rings, but not the supernatant from nonaggregated platelets, also caused contraction. The serotonergic antagonists cyproheptadine, ketanserin, and methysergide caused concentration-dependent inhibition and eventually abolition of contractions evoked by platelets and 5-hydroxytryptamine. Phentolamine and prazosin produced significantly less inhibition of the contractile response to platelets. Pretreatment of the platelets with indomethacin or meclofenamate reduced thromboxane release but had no effect on plateletinduced contractions. Removal of the endothelium did not affect contractile responses to platelets or 5-hydroxytryptamine. These experiments demonstrate that in the canine pulmonary artery: (a) 5-hydroxytryptamine is the predominant mediator of the contractile response triggered by platelet aggregation; and (b) unlike in other blood vessels, the endothelium cannot curtail the contractile response to aggregating platelets.A preliminary report of these findings was published in abstract form (1983. Fed. Proc. 42:593). Introduction 5-Hydroxytryptamine (serotonin) contracts canine and human isolated intrapulmonary vascular preparations (1-4) and elevates pulmonary vascular resistance in intact organisms (5-10) or vascularly isolated perfused lungs (1 1-13). Microembolization or in situ aggregation of platelets produces an elevation of pulmonary vascular resistance, leading to pulmonary hypertension, which can be attributed in part to the release of vasoactive substances (5,(14)(15)(16)(17)(18)(19)

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Section: Discussionmentioning

confidence: 95%