The effects of nifedipine and thapsigargin on the responses of pressurized rat mesenteric artery to 5-hydroxytryptamine and norepinephrine

Abstract

The responses of isolated pressurized second order mesenteric resistance arteries of Wistar rats, superfused with physiological salt solution (PSS) were determined to 5-hydroxytryptamine (5-HT) and norepinephrine (NE). The contractility of the vessel was enhanced in response to 5-HT compared to NE ( P<.001, ANOVA). The L-type calcium ion channel blocker, nifedipine (10 −6 M) abolished the response to either 5-HT or NE. In vessels with intact endothelium, thapsigargin (TG, 10 −6 M), which inhibits uptake of calcium ions into intracellular stores, significantly reduced the contractile response to 5-HT ( P<.02) but had little or no effect on the response to NE ( P=.2). However, in vessels denuded of the endothelium, there was no significant difference in the response of the mesenteric artery, after TG, to either 5-HT or NE. The results indicate that, in the rat mesenteric resistance vessel, both 5-HT and NE use calcium ions from extracellular sources for contraction, while NE relies mainly on extracellular ion influx with little or no contribution from intracellular sources. The reduced response of the de-endothelized vessel to 5-HT after TG suggests that the utilization of intracellular stores by this agonist is endothelium-dependent. These observations may explain the enhanced responsiveness of the mesenteric artery to 5-HT when compared with NE.