Nociceptive vascular reflexes evoked by scorpion venom modulate cardiorespiratory parameters involving vanilloid receptor 1 in anaesthetised rats

Involvement of vanilloid and 5-HT3 receptors in the cardiorespiratory reflexes evoked by intra-arterial (i.a.) injection of Mesobuthus tamulus (BT) venom was examined. In anaesthetised rats, blood pressure, respiratory excursions and ECG were recorded for 60 min after the injection of venom in the absence or presence of antagonists. Injection of BT venom (1 mg/kg, i.a.) produced alterations in respiratory frequency (RF), blood pressure (BP) and heart rate (HR). The changes in RF were manifested as immediate increase (40%) followed by a decrease (40%) and subsequent sustained increase (60%). In case of BP, the increase began around 40 s, peaked at 5 min (50%) and remained above the initial level subsequently. The bradycardiac response began around 5 min which peaked (50% of the initial) around 25 min and remained at that level. Thus, exhibiting immediate-tachypnoeic, intermediate-hypertensive and delayed-bradycardiac responses. Pretreatment with lignocaine, blocked the respiratory responses and attenuated the pressor responses evoked by venom. Pretreatment with capsazepine, vanilloid receptor 1 (VR1) antagonist, antagonized all the three parameters of cardiorespiratory responses evoked by venom. Whereas, ondansetron (5-HT3 antagonist) attenuated the pressor and bradycardiac responses significantly but not the respiratory responses. These observations indicate that the cardiorespiratory changes induced by intra-arterial injection of venom are carried by afferents in addition to somatic nerves, involving mainly VR1 receptors and partially by 5-HT3 receptors.