CARDIOVASCULAR EFFECTS OF BUTHUS-MARTENSII (KARSCH) SCORPION-VENOM

Citation
R. Wang et al., CARDIOVASCULAR EFFECTS OF BUTHUS-MARTENSII (KARSCH) SCORPION-VENOM, Toxicon, 32(2), 1994, pp. 191-200
Citations number
25
Categorie Soggetti
Toxicology,"Pharmacology & Pharmacy
Journal title
ISSN journal
00410101
Volume
32
Issue
2
Year of publication
1994
Pages
191 - 200
Database
ISI
SICI code
0041-0101(1994)32:2<191:CEOB(S>2.0.ZU;2-U
Abstract
Buthus martensii (Karsch) (BMK) scorpion envenomation is a common medi cal problem in China and BMK scorpion has been widely used in traditio nal Chinese medicine. However, the cardiovascular effects of this veno m have not been systematically investigated. In the present study, i.v . BMK venom injection significantly increased the blood pressure in co nscious rats in a concentration-dependent manner (ED(50) = 59 +/- 12 m u g/kg). The increase in blood pressure occurred within 1 min of injec tion of the venom and was sustained for more than 50 min. Heart rate w as not changed by the venom in conscious rats. In vitro studies with B MK venom revealed the increase in the force of contraction, without mo dification of the contraction frequency (within 20 min) of isolated at rial strips. Contractions of isolated arterial strips from aorta, rena l and vertebral arteries were also enhanced by BMK venom with a time l ag of 8 min between the application of the venom and the initiation of the contraction. Furthermore, BMK venom-induced rises in blood pressu re in vivo and increased contraction of isolated vessel strips were in hibited by prazosin and tolazoline, respectively, two alpha(1)-adrener gic antagonists. BMK venom alone did not alter intracellular calcium c oncentrations, [Ca2+](i), in cultured vascular smooth muscle cells and endothelial cells. However, BMK venom significantly increased the met abolism of InsP(3) in dispersed cardiac myocytes, indicating a direct effect on cardiac myocytes. These results demonstrate the significant cardiovascular effects of BMK venom, which may be mediated by an alter ation in InsP(3) in cardiac myocytes but not by [Ca2+](i) in vascular smooth muscle cells.