Intra-arterial (i.a.) injection of Mesobuthus tamulus (BT; 1 mg/kg) venom produces optimal vasosensory reflex responses altering cardiorespiratory parameters in albino rats [1,2]. Since, bradykinin is a constituent of venom therefore, this study was planned to understand the role of kinin receptors in modulating the cardiorespiratory parameters evoked by venom. All the experiments were performed after obtaining the approval from the Institute Ethical Committee for animal experiments. Adult albino rats (200-300g) were anaesthetised with an intra-peritoneal injection of urethane (1.5 g/kg). Tracheostomy was performed to keep the airway patent. Femoral artery was cannulated proximally as well as distally to record the blood pressure and to inject the chemicals, respectively. Blood pressure (BP), electrocardiogram (ECG) and respiration (RR) was recorded in presence or absence of antagonists. After i.a. injection of venom there was immediate (within 2 s) increase in RR which reached to 40% within 30 s, followed by a decrease of 40% from initial. Further, there was sustained increase in RR (50%) up to 60 min. The BP began to increase at 40 s, peaking at 5 min (50%) and remained above the initial level up to 60 min. The bradycardiac response started after 5 min which peaked (50%) at 25 min and remained at that level up to 60 min. In des-Arg (B1 receptor antagonist; 10 ng/kg) pre-treated animals, the venom induced respiratory changes were similar to the venom only group but venom induced cardiovascular responses attenuated (20-25% in MAP and HR) significantly (P < 0.05, Two way ANOVA). In Hoe-140 (B2 receptor antagonist; 10 ng/kg) pre-treated group, the venom induced respiratory changes were similar to the venom only group but venom induced BP responses attenuated (~25%) from 30-60 min (P < 0.05, Two way ANOVA) and HR responses accentuated (25-50%) up to 15 min significantly (P < 0.05). Thus, i.a. injection of venom produces immediate hyperventilatory, intermediate hypertensive and delayed bradycardiac responses. BT venom contains serotonin, histamine, bradykinin potentiating factor, peptide toxins, etc which is a potential nociceptive agents [3]. Bradykinin (BK) is an inflammatory mediator and produces the actions involving B1 and B2 receptors [4]. Involvement of kinin and prostaglandin (PG) to noxious stimulation has been shown [5]. In the present study, the B1 antagonist pre-treatment attenuated the venom induced BP and heart rate changes indicating the B1 receptors involvement in producing the responses. These observations are consistent for the B1 receptor involvement in the nociception. However, the involvements of B2 receptor on venom induced cardiorespiratory parameters are less evident in this study.