PMID: 7539591May 1, 1995Paper

Inhibitory effect of indomethacin on prostacyclin receptor-mediated cerebral vascular responses

The American Journal of Physiology
Helena ParfenovaC W Leffler

Abstract

The present study addresses the hypothesis that indomethacin, in addition to blocking prostaglandin synthesis, directly inhibits prostacyclin receptor-mediated cerebral vascular responses. To test this hypothesis, the effects of indomethacin on pial arteriolar dilation in response to the prostacyclin receptor agonist iloprost were investigated using a cranial window technique in newborn pigs. Topically applied iloprost resulted in dose-dependent pial arteriolar dilation and concomitant increases in cortical adenosine 3',5'-cyclic monophosphate (cAMP). Indomethacin (5 mg/kg iv + 10(-4) M topically) greatly reduced both the vasodilation and the increase in cortical cAMP in response to iloprost. In contrast, indomethacin did not attenuate beta-adrenoreceptor-mediated vasodilation and the increase in cortical cAMP in response to isoproterenol. Aspirin (50 mg/kg iv + 10(-3) M topically) did not affect pial arteriolar dilation or the increase in cortical cAMP in response to iloprost. Unlike indomethacin, aspirin was not effective in inhibiting prostanoid-associated cerebral vasodilation and increase in cortical cAMP in response to hypercapnia. The present data suggest that indomethacin selectively inhibits prostacyclin receptor-media...Continue Reading

Citations

Nov 29, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Julian H LombardJefferson C Frisbee
Feb 10, 2006·Journal of Applied Physiology·Charles W LefflerRui Wang
Mar 15, 2001·American Journal of Physiology. Heart and Circulatory Physiology·C W LefflerA L Fedinec
Sep 15, 2001·American Journal of Physiology. Heart and Circulatory Physiology·J C FrisbeeJ H Lombard

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