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(Hypertension. 2005;45:1068.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Loss of Vascular Regulation by Soluble Guanylate Cyclase Is Emerging as a Key Target of the Hypertensive Disease Process

Michael S. Wolin

From the Department of Physiology, New York Medical College, Valhalla, NY.

Correspondence to Michael S. Wolin, PhD, Department of Physiology, Basic Science Building, Room 604, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin@nymc.edu

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

The soluble form of guanylate cyclase (sGC) is well established as a primary target for the actions of NO. It is a key regulator of vascular smooth muscle force and growth through its production of cGMP. In this issue of Hypertension, Klöss et al¹ provide evidence that aged hypertensive rats have decreased levels of an mRNA-binding protein human R (HuR), which stabilizes the mRNA for the subunits of sGC and enables expression of this important enzyme. Previous work from this group showed how the HuR protein functions to stabilize the mRNA for sGC² and that the expression of HuR is controlled by the availability of cGMP, whereas cGMP appears to inhibit the expression of this mRNA-stabilizing protein.³ Because hypertension is thought to generally decrease sGC expression and the stimuli for sGC activation,^4,5 the decrease in HuR expression is likely to be through a mechanism that is independent of the previously identified interactions of cGMP with this system. A model describing the potential influence of hypertension on relationships between these systems in controlling the expression and activity of sGC is shown in the Figure. The decrease in HuR has many implications for controlling processes potentially involved in the progression of hypertension that are discussed in the article by Klöss et al.¹ However, the influence of HuR on the expression of sGC may be a primary factor in the progression of hypertension. cGMP generated by sGC appears to coordinate multiple signaling mechanisms that control vascular force and processes involved in . . . [Full Text of this Article]

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Human-Antigen R (HuR) Expression in Hypertension: Downregulation of the mRNA Stabilizing Protein HuR in Genetic Hypertension

Stephan Klöss, Daniela Rodenbach, Reingart Bordel, and Alexander Mülsch
Hypertension 2005 45: 1200-1206. [Abstract] [Full Text] [PDF]

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