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(Hypertension. 2004;44:25.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

C3 or Not C3

That Is the Question

From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing.

Correspondence to Stephanie W. Watts, PhD, B445 Life Sciences Building, Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317. E-mail wattss@msu.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Numerous investigators have studied the potential genetic causes of essential hypertension, and several genes have been described as candidates.^1,2 These genes may contribute to the inappropriate and exaggerated growth of arterial smooth muscle cells in genetically hypertensive individuals and thus ultimately contribute to the disease by supporting creation of stronger, more muscular, and sometimes narrowed arteries. The article by Lin et al in this issue of Hypertension³ describes selective expression of the complement protein complement 3 (C3) in arterial cells from the spontaneously hypertensive rat (SHR) and clear involvement of this protein in mediating enhanced arterial smooth muscle growth in the SHR.

Complement 3

The complement system is a major effector of humoral immunity and innate immunity. Complement proteins, normally found in the plasma, are inactive and become active through classical stimulation (antibody-activated) pathways or alternative (cell surface–activated) pathways. Proteolysis of C3 represents an early and essential event in complement activation through either pathway. Cleavage of C3 by spontaneous breakdown, binding to a microbial surface, or through binding a C3 convertase leads to generation of 2 proteolytic proteins called C3a and C3b. These effectors act ultimately to cause phagocytosis of opsonized particles, activate later stages of complement (through formation of C5 convertase), and induce inflammation.⁴

The possible role of C3 or complement in hypertension has largely been studied in the kidney, where C3 or complement plays a role in IgA nephropathy,⁵ is deposited in small arteries and arterioles of SHRs given deoxycorticosterone acetate (DOCA) and salt,⁶ and is necessary for renal injury . . . [Full Text of this Article]