Evidence of mammalian Ca 2+ channel inhibitors in venom of the spider Plectreurys tristis

Abstract

P. M. Lundy and R. Frew. Evidence of mammalian Ca 2+ channel inhibitors in venom of the spider Plectreurys tristis. Toxicon 31, 1249–1256, 1993.— Plectreurys tristis venom inhibited K +-stimulated Ca 2+ influx in a concentration-dependent manner in rat (0.5–4.0 μg venom protein/ml) and chicken (1.0–64.0 μg venom protein/ml) brain synaptosomes. In contrast to Hololena curta venom or omega conotoxin GV1A which both show selectivity for avian synaptosomes, inhibition of Ca 2+ influx by the venom appeared to be relatively selective for rat synaptosomes. Plectreurys tristis venom also inhibited K +-evoked release of [ 3H](-)-noradrenaline from labeled rat cortical synaptosomes. Responses to electric field stimulation of the sympathetically innervated rat vas deferens in vitro were inhibited by Plectreurys tristis venom at dilutions similar to those which inhibited Ca 2+ influx in synaptosomes. Inhibition persisted following washout of the venom. K +-evoked contractions of rat aortic rings were relaxed by the dihydropyridine antagonist (-)-202–791, but not by Plectreurys tristis venom, thus precluding an effect on K +-depolarized smooth muscle L-type channels. Contractions to exogenous (-)-noradrenaline in rat aorta were not inhibited by Plectreurys tristis venom, ruling out an effect on α 1-adrenergic receptors, and further suggesting a prejunctional site of action. The results suggest that this venom inhibits N-type Ca 2+ channels, as well as unclassified Ca 2+ channels, which are neither N- nor L-type.