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Summary It is proposed here that a deficiency of BK might be a significant factor in the pathophysiology of hypertension and diabetes. In this regard, it is suggested that the role of renal BK is to excrete the excess sodium. Therefore, a reduction in the generation of renal BK may be the cause for the development of hypertension as a result of the accumulation of sodium in the body. Thus, the development of a compound having renal kallikrein-like activity may serve the purpose of excreting excessive sodium from the kidney in the treatment of hypertension. Transgenic mice over-expressing renal tissue kallikrein were hypotensive and that administration of aprotinin, a tissue kallikrein inhibitor, restored the BP of the transgenic mice. Recently, it has been proposed that tissue kallikrein gene delivery into various hypertensive models exhibits protection, such as reduction in high blood pressure, attenuation of cardiac hypertrophy, inhibition of renal damage and stenosis. This may indicate the future therapeutic aspect of kallikrein gene therapy for hypertension, cardiovascular and renal pathology.

An Overview on Relation between the Bradykinin System and Hypertension and Diabetes