[Role of the blood kallikrein-kinin system in activating hemodynamic effects induced by L-thyroxine].

Intravenous injection of large L-thyroxine doses (200 micrograms/100 g) was shown to activate kinin formation and to reduce arterial pressure by 33% in experimental white rats. It was established that sensitivity of bradykinin receptors increases during experimental thyrotoxicosis. During kininogenesis inhibition with contrykal, a kallikrein inhibitor, as well as during the kinin system components deficiency, intravenous injection of the same thyroxine doses did not result in arterial pressure changes. The results obtained suggest that hypotensive effect of thyroxine is mediated via the kallikrein kinin system.