Trachte G J, Stein E A
Department of Pharmacology, University of Minnesota-Duluth, School of Medicine.
J Pharmacol Exp Ther. 1989 Apr;249(1):216-20.
Two thromboxane receptor agonists, carbocyclic thromboxane A2 (CTA) and 9,11-dideoxy-11,9-epoxymethano prostaglandin F2 alpha (U46619), were examined for their influence on basal force and electrically induced force of isolated superior mesenteric arterial rings from rabbits. Both CTA and U46619 contracted the arterial rings and augmented contractile responses to electrical stimulation (4-20 Hz). The CTA and U46619 also augmented contractile responses to norepinephrine (P less than .05) and enhanced norepinephrine release in response to a 16 Hz electrical stimulation (P less than .05). The increases in basal force, neurogenic responses and norepinephrine release were prevented by the thromboxane receptor antagonist, (1S-[1-alpha,2-beta(5Z),3-beta, 4-alpha])-7-[3- [(2- [(phenylamino)carbonyl]hydrazino]methyl]-7- oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid. The U46619 was more potent than CTA and had a more consistent effect on norepinephrine release. These results are consistent with the hypothesis that thromboxane receptor agonists augment adrenergic neurogenic responses via thromboxane receptors. The mechanism of the enhanced neurogenic responses involved both pre- and postjunctional effects of the thromboxane receptor agonists.
研究了两种血栓素受体激动剂，即环戊烷血栓素A2（CTA）和9,11-二脱氧-11,9-环氧甲撑前列腺素F2α（U46619）对兔离体肠系膜上动脉环基础张力和电诱导张力的影响。CTA和U46619均使动脉环收缩，并增强对电刺激（4 - 20Hz）的收缩反应。CTA和U46619还增强对去甲肾上腺素的收缩反应（P < 0.05），并增强对16Hz电刺激的去甲肾上腺素释放（P < 0.05）。血栓素受体拮抗剂（1S-[1-α,2-β(5Z),3-β,4-α])-7-[3-[(2-[(苯基氨基)羰基]肼基]甲基]-7-氧杂双环[2.2.1]庚-2-基]-5-庚烯酸可阻止基础张力、神经源性反应和去甲肾上腺素释放的增加。U46619比CTA更有效，对去甲肾上腺素释放的作用更一致。这些结果与血栓素受体激动剂通过血栓素受体增强肾上腺素能神经源性反应的假说一致。神经源性反应增强的机制涉及血栓素受体激动剂的节前和节后效应。
