Human Tissue Kallikrein Activity in Angiographically Documented Chronic Stable Coronary Artery Disease.

Background: Human tissue kallikrein (hK1) is a key enzyme in the kallikrein-kinin system (KKS). hK1-specific amidase activity is reduced in urine samples from hypertensive and heart failure (HF) patients. The pathophysiologic role of hK1 in coronary artery disease (CAD) remains unclear.

Increased tissue kallikrein amidase activity in urine of patients with type 1 diabetes under insulin therapy, and in those with gestational diabetes mellitus not under insulin therapy.

Human tissue kallikrein (hK1) is reduced in hypertension, cardiovascular and renal diseases. There is little information on the participation of hK1 in type 1 diabetes mellitus (DM), type 2 DM, and gestational diabetes mellitus (GDM), respectively. The aim of this study was to evaluate the roles of insulin and hyperglycemia on urinary hK1 activity in type 1 DM and in GDM.

On human tissue kallikrein activity in urine of Brazilian White and Black primary hypertensive patients.

Objective: To evaluate the possible relationship between the human tissue kallikrein amidase activity with sex and ethnicity in Brazilian primary hypertensive patients.

Design: Population-based study.

Participants: One hundred men and women, Black and White primary hypertensive patients aged 20 years and older were selected.

The amidase activity of human tissue kallikrein is significantly lower in the urine of patients with systolic heart failure.

Background: Heart failure (HF) is a clinical syndrome that activates several neurohumoral systems. There is little information on the participation of renal kallikrein-kinin system (KKS) in HF. Kallikreins are key enzymes in this system.

The effect of cations on the amidase activity of human tissue kallikrein: 1-linear competitive inhibition by sodium, potassium, calcium and magnesium. 2-linear mixed inhibition by aluminium.

Hydrolysis of D-valyl-L-leucyl-L-arginine p-nitroanilide by human tissue kallikrein (hK1) was studied in the absence and in the presence of increasing concentrations of the following chloride salts: sodium, potassium, calcium, magnesium and aluminium. The data indicate that the inhibition of hK1 by sodium, potassium, calcium and magnesium is linear competitive and that divalent cations are more potent inhibitors of hK1 than univalent cations. However the inhibition of hK1 by aluminium cation is linear mixed, with the cation being able to bind to both the free enzyme and the ES complex.