Abstract
The aim of our research is to study the effect relaxant action of diterpenoid alkaloids talatisamine, 14-O-benzoylthalatisamine and 14-O-acetylthalatisamine was studied using isolated rat aortic rings. Alkaloids significantly and dose-dependently inhibited contraction of the aortic rings caused by high KCl content. At the same time, under these conditions, alkaloids significantly reduced Ca2+-induced contraction of the aortic rings. The relaxing effects of alkaloids are significantly suppressed by verapamil, a potent potentiometer-dependent Ca2+ channel blocker. The alkaloids also significantly reduced norepinephrine-induced aortic ring contraction in normal as well as Ca2+ free Krebs solutions. The data obtained indicate that talatisamine, 14-benzoylthalatisamine and 14-O-acetylthalatisamine exhibit a pronounced relaxant effect in almost the same way in the case of contraction induced by a high content of KCl and norepinephrine. The mechanism of the relaxant action of alkaloids is probably complex and may include suppression of Ca2+influx through voltage-dependent and receptor-driven Ca2+ channels, as well as inhibition of Ca2+transport in the sarcoplasmic reticulum.
Highlights
Ca2+ ions play a leading role in ensuring the functional activity of blood vessel SMC
We have previously found that the alkaloid 14-O-benzoylthalatizamine (14-O-BT), a derivative of the diterpenoid alkaloid talatizamine isolated from the plant Aconitum talassicum, effectively relaxes the preparations of the aorta, previously contracted by KC1 [5]
To assess the effect of the studied alkaloids on receptor-gated Ca2+ channels, we studied their effects on the contractions of aortic preparations induced by the α-adrenergic receptor agonist phenylephrine (PE)
Summary
Ca2+ ions play a leading role in ensuring the functional activity of blood vessel SMC. The contractile activity of SMCs depends on [Ca2+]i, the mechanisms involved in its regulation in SMCs have their own characteristics In this case, the dominant role is played by potential-dependent Ca2+ -channels of the plasma membrane, the activation of which provides the flow of Ca2+ ions into the cytoplasm of the SMC, the amount of which is sufficient to initiate the contractile process [1]. In addition to voltage-dependent Ca2+ channels, the supply of Ca2+ from the extracellular environment to the SMC is provided by a supply - detectable and receptor-gated Ca2+ channels, as well as a Na+ / Ca2+ exchanger [2]. In SMCs such activation of phospholipase C is accompanied by the production of inositol 1,4,5triphosphate (IP3), which interacts with the receptor (IP3R) on the CP membrane, activates the release of Ca2+ and causes an increase in [Ca2+] i in their cytoplasm [4]
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