Open AccessAliskiren-Binding Increases the Half Life of Renin and Prorenin in Rat Aortic Vascular Smooth Muscle Cells
Author(s) -
Wendy W. Batenburg,
René J.A. de Bruin,
Jeanette M.G. van Gool,
Dominik N. Müller,
Michael Bäder,
Geneviève Nguyen,
A.H. Jan Danser
Publication year - 2008
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.108.164210
Subject(s) - aliskiren , renin inhibitor , renin–angiotensin system , endocrinology , receptor , medicine , chemistry , plasma renin activity , vascular smooth muscle , angiotensin ii , pharmacology , biology , smooth muscle , blood pressure
Renin inhibition with aliskiren has been reported to cause a greater rise in renin than other types of renin-angiotensin system blockade, thereby potentially leading to angiotensin generation or stimulation of the human (pro)renin receptor (h(P)RR). Here we studied whether this rise in renin is attributable to an aliskiren-induced change in the prorenin conformation, allowing its detection in renin assays, or a change in renin/prorenin clearance. We also investigated whether aliskiren affects (pro)renin binding to its receptors, using rat aortic vascular smooth muscle cells (VSMCs) overexpressing the h(P)RR.
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