Mallow D, Ludwig D, Nilson G. 2003. True Vipers: Natural History and Toxinology of Old World Vipers. Krieger Publishing Company, Malabar, Florida. 359 pp. ISBN 0-89464-877-2.
also interseting: In the guinea-pig Langendorff heart preparation, addition of 0.1 mg Bitis nasicornis venom to the perfusion solution caused transient increases in heart rate (HR) and left ventricular systolic pressure (LVSP) with peak increases at 2 min. With higher doses (0.6 and 1.4 mg), these increases were followed by the return of HR to normal, significant decreases in LVSP below control values and marked increases in left ventricular diastolic pressure. Histaminergic blockade with ranitidine reduced the positive responses. The results suggest that a venom component, possibly acting on intracellular calcium movement, could be responsible for both positive and negative effects.
Venom from B. nasicornis, but not from Bitis arietans, Echis carinatus or Cerastes cerastes, produced an irreversible contraction of the isolated aortic strip that was slow in onset, increased with time, and reached maximum in about 10 – 15 min. The contraction was not inhibited by pretreatment with atropine, yohimbine, phentolamine, cyproheptadine or indomethacin, however, it was blocked by incubation in a Ca2+-free solution and was partially blocked by incubation with the Ca2+ channel blockers verapamil and nifedipine. It is concluded that B. nasicornis venom may act by increasing the Ca2+ influx into smooth cells, thus causing an increase in intracellular Ca2+ concentration and hence a contraction of the aortic strip.
