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JCI table of contents: Aug. 16, 2007
Date:8/16/2007

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TITLE: Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency

AUTHOR CONTACT: Charles L. Sawyers Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Phone: (646) 888-2138; Fax: (646) 888-2595; E-mail: sawyersc@mskcc.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=30890


EDITOR'S PICK: Specific antagonism lowers blood pressure

High blood pressure (hypertension) is associated with an increased risk of heart attack and stroke, and the frequent use of drugs known as NSAIDs, for example to treat individuals with rheumatoid arthritis, can cause hypertension. Exactly why NSAIDs cause hypertension is not clear because they inhibit the generation of several soluble factors (known as prostaglandins) that can affect blood pressure and the effects of inhibiting the individual receptors for prostaglandins are not known. In an attempt to address this issue researchers from Vanderbilt University Medical Center identified a novel potential target for the treatment of hypertension.

In the study, which appears online on August 16 in advance of publication in the September print issue of the Journal of Clinical Investigation, Matthew Breyer and colleagues show that inhibitors of the prostaglandin E2 receptor EP1 reduce hypertension in rats. Consistent with this, mice lacking EP1 were protected from the hypertensive effects of angiotensin II and EP1-specific agonists. The authors therefore suggest that targeting the PGE2 receptor EP1 might be a viable approach to treating hypertension.

TITLE: Antihypertensive effects of selective prostaglandin E2 receptor subtype 1 targeting

AUTHOR CONTACT: Matthew D. Breyer Vanderbilt University Medical Center, Nashville, Tennessee, USA. Phone: (615) 343-
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Contact: Karen Honey
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Journal of Clinical Investigation
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