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1 The actions of the cannabinoid receptor antagonist, SR 141716A, were examined in rat isolated mesenteric arteries. At concentrations greater than 3 μM, it caused concentration‐dependent, but endothelium‐independent, relaxations of both methoxamine‐ and 60 mM KCl‐precontracted vessels. 2 SR 141716A (at 10 μM, but not at 1 μM) inhibited contractions to Ca2+ in methoxamine‐stimulated mesenteric arteries previously depleted of intracellular Ca2+ stores. Neither concentration affected the phasic contractions induced by methoxamine in the absence of extracellular Ca2+. 3 SR 141716A (10 μM) caused a 130 fold rightward shift in the concentration‐response curve to levcromakalim, a K+ channel activator, but had no effect at 1 μM. 4 SR 141716A (10 μM) attenuated relaxations to NS 1619 (which activates large conductance, Ca2+‐activated K+ channels; BKCa). The inhibitory effect of SR 141716A on NS 1619 was not significantly different from, and was not additive with, that caused by a selective BKCa inhibitor, iberiotoxin (100 nM). SR 141716A (1 μM) did not effect NS 1619 relaxation. 5 SR 141716A (10 μM) had no effect on relaxations to the nitric oxide donor S‐nitroso‐N‐acetylpenicillamine, or relaxations to carbachol in the presence of 25 mM KCl. 6 The results show that, at concentrations of 10 μM and above, SR 141716A causes endothelium‐independent vasorelaxation by inhibition of Ca2+ entry. It also inhibits relaxations mediated by K+ channel activation. This suggests that such concentrations of SR 141716A are not appropriate for investigation of cannabinoid receptor‐dependent processes. British Journal of Pharmacology (1998) 125, 689–696; doi:10.1038/sj.bjp.0702127
British Journal of Pharmacology – Wiley
Published: Oct 1, 1998
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