Indian red scorpion (Buthus tamulus) venom-induced augmentation of cardiac reflexes is mediated through the mechanisms involving kinins in urethane anaesthetized rats.

The mechanism underlying the action of Indian red scorpion (Buthus tamulus; BT) venom on cardiac reflexes was examined in urethane anaesthetized adult albino rats of either sex. Intravenous injection of phenyldiguanide (PDG) produced reflex hypotension, bradycardia and apnea lasting for > 60 s. The PDG-induced reflex responses (blood pressure, heart rate and respiration) were augmented greatly (magnitude and time period) after exposure to BT venom (100 microg/kg, i.v., for 30 min). However, there were no great alterations in resting blood pressure, heart rate and respiratory rate. Pretreatment with kallikrein kinin inhibitor (aprotinin; 6000 kallikrein inactivating unit, i.v.) blocked the BT venom-induced augmentation of PDG reflex response. Further, pretreatment with indomethacin (prostaglandin synthetase inhibitor; 10 mg/kg) and heparin (1000 units/kg) also blocked the venom-induced potentiation of the reflex. Captopril (15 mg/kg), an agent known to increase endogenous kinins, also augmented the PDG induced-reflex to the same extent as in BT envenomed rats. The captopril-induced augmentation of the reflex was blocked by aprotinin and heparin, but not by indomethacin. The results indicate that kinins and prostaglandins are involved in the BT venom-induced augmentation of the cardiac reflexes.