Summary
Kallikrein exists in plasma in both active (kallikrein) and precursor forms (kallikreinogen). The active form was measured by the spontaneous hydrolysis of N-α tosyl-L-arginine methylester (TAME) by untreated plasma, and the total kallikrein activity was measured by TAME hydrolysis after activation of plasma with kaolin. The amount of precursor present was obtained by subtraction of these two values.
The daily investigation of kallikrein activity in the plasma of splenectomised calves infected with Babesia argentina by these techniques showed that the rate of conversion of kallikreinogen to kallikrein increased one to two days before parasites were detectable in peripheral blood and that this continued until the reserves of kallikreinogen fell to less than 10% of normal levels 11–12 days after the day of infection. Deaths characterised by clinical signs of shock occurred at this stage. These data supported an earlier conclusion (Wright, 1973a) that kallikrein played an important role in the terminal shock observed in B. argentina infection. The increased conversion of prekallikrein to kallikrein was closely correlated with the early growth aud multiplication of the parasites in peripheral blood. Tissue damage alone of the magnitude caused by the early destruction of red cells in babesiosis did not cause significant activation of the kallikrein system and a substance(s) released by parasites was postulated as a possible cause.
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Wright, I.G., Mahoney, D.F. The activation of kallikrein in acute babesia argentina infections of splenectomised claves. Z. Parasitenk. 43, 271–278 (1974). https://doi.org/10.1007/BF00328881
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DOI: https://doi.org/10.1007/BF00328881