Confirmation of direct angiotensin formation by kallikrein

‏‎suppression of coke formation in thermal cracking by coke inhibitors‎‏

‏‎the main purpose of this research was to:1.develop a coking model for thermal cracking of naphtha.2.study coke inhibition methods using different coke inhibitors.developing a coking model in naphtha cracking reactors requires a suitable model of the thermal cracking reactor based on a reliable kinetic model.to obtain reliable results all these models shall be solved simultaneously.for this pu...

Tissue kallikrein elicits cardioprotection by direct kinin b2 receptor activation independent of kinin formation.

Tissue kallikrein exerts various biological functions through kinin formation with subsequent kinin B2 receptor activation. Recent studies showed that tissue kallikrein directly activates kinin B2 receptor in cultured cells expressing human kinin B2 receptor. In the present study, we investigated the role of tissue kallikrein in protection against cardiac injury through direct kinin B2 receptor...

Direct action of kallikrein and other proteases on the renin-angiotensin system.

Kallikrein is present in the renal tubule near the macula densa, and it has recently been shown to activate inactive renin in human plasma. We recently showed that kallikrein was a potent stimulus of renin release and increased renin secretion in a dose-dependent fashion. To study its effect on renal renin release, we superfused rat renal cortical slices with purified rat urinary kallikrein. Ka...

Impact of Renin-Angiotensin- and Kallikrein-Kinin Systems in Aneurysm Formation and Possible Therapeutic Implications

Formation of angiotensin III by angiotensin-converting enzyme.

Angiotensin III is formed from des-Asp1 -angiotensin I by angiotensin-converting enzyme. The Km (11 muM) of the reaction is one-third of that for the conversion of angiotensin I into angiotensin II. As suggested by the Km values, bradykinin, peptide BPP9a and angiotensins II and III are better inhibitors of the formation of angiotensin II than of the formation of angiotensin III.