The present study was designed to examine the effects of venom from the scorpion Leiurus quinquestriatus hebraeus (Lqh) on the contractility of rat aortic rings. We first examined the effect of Lqh venom on the contractile tension of isolated rat vascular aortic rings and then whether long-term exposure to the venom reduces the contractility of vascular smooth muscle by increasing the production of nitric oxide. Following the administration of 33 μg/mL of crude Lqh venom, contractile tension increased by 18.9 ± 11.4 percent. The administration of 2.4 × 10-7 M noradrenaline (NA) led to a 31.6 ± 8.2 percent increase in tension (p <0.01). The effects induced by NA and Lqh venom were similar and additive (p <0.01). Pretreatment with the alpha-adrenergic blocker phenoxybenzamine (0.2 μM) eliminated the effect of the venom, whereas the calcium-channel blocker verapil (8.3 μM) merely attenuated the effect. Incubation of the rings with Lqh venom for 16 to 18 h, followed by NA stimulation, led to a 15 to 20 percent decrease in tension (p <0.001). Treatment with N-omega-nitro-L-arginine methyl ester (110 μM), a constitutional nitric oxide inhibitor, restored the tension to control values. Treatment with S-methyl-isothiourea (0.1 |iM), an inducible nitric oxide synthesis inhibitor, had no effect on contractile tension. The results of the present study suggest that the effect of Lqh venom on isolated aortic rings is induced via sympathetic nerve terminals. Calcium had little effect on the smooth muscle contractility of aortic rings incubated with the venom. No evidence was found to support nitric oxide synthesis after the long-term exposure of the rings to Lqh venom.
|Number of pages||14|
|Journal||Journal of Basic and Clinical Physiology and Pharmacology|
|State||Published - 2003|
- nitric oxide
- scorpion venom