Palytoxin-induced K+ efflux from ileal longitudinal smooth muscle of the guinea-pig.
スポンサーリンク
概要
- 論文の詳細を見る
In guinea-pig ileal longitudinal smooth muscle, both palytoxin (PTX) and carbachol (CCh) increased K<SUP>+</SUP> efflux with an EC50 of 1.8×10<SUP>-10</SUP> M and 4.1×10<SUP>-7</SUP> M, respectively. Atropine (10<SUP>-6</SUP> M) did not inhibit the K<SUP>+</SUP> efflux due to PTX (3×10<SUP>-9</SUP> M), but completely inhibited the efflux due to CCh (10<SUP>-5</SUP> M). External Ca<SUP>2+</SUP> removal and verapamil (10<SUP>-5</SUP> M) did not change the PTX-induced K<SUP>+</SUP> efflux, although the CCh-induced K<SUP>+</SUP> efflux was inhibited about 77% and 71%, respectively. PTX-induced K<SUP>+</SUP> efflux was reduced to 31% by a depletion of intracellular Ca<SUP>2+</SUP>. Tetraethylammonium (15 mM) inhibited the K<SUP>+</SUP> efflux due to PTX or CCh to 61% or 75%, respectively. The PTX-induced K<SUP>+</SUP> efflux was also inhibited by cymarin (3×10<SUP>-8</SUP> M), ouabain (10<SUP>-5</SUP> M) and digitoxin (10<SUP>-5</SUP> M). These results suggest that the PTX-induced K<SUP>+</SUP> efflux is less dependent on Ca<SUP>2+</SUP> influx than that due to CCh. Furthermore, the binding sites for PTX in the ileal muscle of guinea-pig may be Na<SUP>+</SUP>, K<SUP>+</SUP>-ATPase, as has been suggested in other types of cells.
- 公益社団法人 日本薬理学会の論文
公益社団法人 日本薬理学会 | 論文
- Neurotoxin A2NTX Blocks Fast Inhibitory and Excitatory Transmitter Release From Presynaptic Terminals
- Loxiglumide, L - 364,718 and L - 365,260 Prevent the Inhibition of Spontaneous Acetylcholine Release from the Frontal Cerecral Cortex of Freely Moving Rat Peripherally Administered with Cholecystokinin - 8S
- A new device for the determination of microsomal cytochrome P-450 in renal tissue preparations from various species contaminated with mitochondria and hemoglobin.
- Leukocyte Recruitment to Peritoneal Cavity of Rats Following Formalin Injection : Role of Tachykinin Receptors
- Immunopharmacologic studies of D-penicillamine-L-cysteine disulfide.