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α‐AND β‐ADRENOCEPTOR AGONIST ACTIVITY IN THE VENOM OF THE AUSTRALIAN HUNTSMAN SPIDERS, DELENA CANCERIDES AND ISOPEDA MONTANA
Author(s) -
Korszniak N. V.,
Story D. F.
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb00585.x
Subject(s) - venom , agonist , chemistry , pharmacology , biology , receptor , medicine , ecology
SUMMARY 1. Crude venom gland extracts (VGE) were prepared from female Delena cancerides and Isopeda montana spiders. The VGE were tested in isolated rat atrial, caudal artery and pithed rat preparations for pharmacological activity. 2. In rat isolated atrial preparations, D. cancerides and I. montana VGE, each in a concentration of 2 glands/mL, produced increases in atrial rate which were abolished by propranolol (1 μmol/L) but not by ketanserin (0.1 μmol/L) or reserpine pretreatment (2.5 mg/kg s.c. 24 h prior to experimentation) indicating a direct action on atrial β‐adrenoceptors. 3. In rat caudal artery preparations each VGE produced an increase in perfusion pressure, which was taken as an index of vasoconstriction. Pressor responses to D. cancerides VGE (1 gland/mL) were abolished in the presence of prazosin (1 mol/L) but not by reserpine pretreatment, indicating an action of the VGE on vascular α 1 ‐adrenoceptors. Neither prazosin nor reserpine pretreatment had any effect on pressor responses of rat caudal artery preparations to I. montana VGE. Ketanserin (6 nmol/L) produced a small reduction in the degree of vasoconstriction produced by the VGE. This demonstrates a lack of α 1 ‐adrenoceptor agonist activity of the VGE. 4. Both VGE produced dose‐dependent increases in mean arterial pressure and heart rate in pithed rat preparations. The use of relatively selective receptor antagonists indicated that the increases in mean arterial pressure (MAP) produced by both VGE were mediated by an action on α 2 ‐adrenoceptors.