Abstract

Palytoxin (Palythoa tuberculosa)(PTX) in concentration higher than 10 M increased tissue Na and decreased tissue K contents in smooth muscle of rabbit aorta. Thegexchange of extracellular Na with intracellular K induced by PTX (10 M) was completed within Ih. Saponin (1mg/ml) and TritonX-100(0.1%wt/vol) also rapidly decreased tissue K content. On the other hand,high concentration of ouabain (10-3 M) did not change the tissue K content within one hour of application, and the maximum loss of K was obtained after 6h. Lgss of tissue Na into Na- and K-free solution was accelerated by PTX (10 M). The PTX-induced increase in loss of Na was inhibited in proportion to decrease in the temperature from 37 to 10 °C, while the loss of Na in the absence of PTX was almost completely inhibited at 24 °C. Decrease in the wet weight of the muscle induced by hyperosmotic solution was inhabited by pretreatment with PTX (10 M). PTX in concentration above 10 M reduced the ATP content, and significant amount of ATP was detected in the incubation medium. Saponin (lmg/ml) and TritonX-100 (0.1%) induced a release of Na from liposome prepared with synthesized lecithin or total lipids of^rabbit red blood cells. However, no Na leak was induced by PTX (10 -10 M) in ^hesegliposomes. These results suggest that PTX at low concentration (10 -10 M) increases membrane permeability to Na and K_i,ons_gf the vascular smooth muscle cells. At higher concentration (10 -10 M), it seems to form pores which are permeable to a larger molecule like ATP. The effects might not be mediated through the interaction with membrane lipids.

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