EFFECT OF ACL MYOTOXIN ON THE WATER TRANSPORT IN THE ISOLATED TOAD URINARY BLADDER

Leite, R. S.; Selistre-de-Araujo, H. S.; Franco, W.

Departamento de Ciências Fisiológicas UFSCar, São Carlos, SP, Brazil.

Phospholipase A₂-like myotoxins induce necrosis of skeletal muscle cells by a not well understood mechanism. There are evidences in the literature that these myotoxins influence directly or indirectly the hydromineral transport in biological tissues. Myotoxin ACL belongs to the family of the K49PLA₂, purified from Agkistrodon contortrix laticinctus venom, which increases the basal water transport and promotes a decrease of the vasopressin hydrosmotic effect in this epithelium. These effects could be mediated, in part, by an increase of cytossolic calcium. Thus, the objective of the present work was to study the role of the Ca⁺² ion in the myotoxin ACL hydrosmotic action in presence of calcium antagonists in the toad bladder in vitro. Water flow was measured gravimetrically by Bentley’s technique (J. Endocrinol. 17: 201-209, 1958) using an osmotic gradient of 4 atm in hemibladders from same animal. Control hemibladders were treated with myotoxin (10nM) and experimental hemibladders received myotoxin plus lanthanum (50mM). Water flow was 3,13±0,35ml/min (n=7) and 1,42±0,25 ml/min respectively, and the difference was significant (p<0,01) between these values. This result shows a decrease of 54% in the myotoxin hydrosmotic action. In other experiments, control group was treated myotoxin and the experimental group received myotoxin associated with nifedipine(10mM) resulting in a water flow 2,96±0,49ml/min (n=8) and 1,81±0,20ml/min respectively, showing a decrease of 38% of the myotoxin hydrosmotic effect. The results suggest that ACL myotoxin increases cytossolic calcium through the release of Ca⁺² stored in the endoplasmic reticulum and also by an increase of the influx these ions via nifedipine sensitive channels.

Financial support: CAPES

CORRESPONDENCE TO:

Renner de Souza Leite, Porto Rico 1604, São Carlos, SP, CEP: 13566730, Brasil, Email: rennerleite@zipmail.com.br