This Article Full Text Full Text (PDF) All Versions of this Article: 46/5/e18    most recent 01.HYP.0000188174.83586.20v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cai, T. Articles by Joe, B. Search for Related Content PubMed PubMed Citation Articles by Cai, T. Articles by Joe, B. Related Collections Other hypertension Other etiology

(Hypertension. 2005;46:e18.)
© 2005 American Heart Association, Inc.

Hypertension Electronic Pages

Are IA-2 and RESP18 Involved in Trait of Blood Pressure?

Experimental Medicine Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research/National Institutes of Health, Bethesda, Maryland

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

To the Editor:

Congenic rat strains are important tools for the genetic dissection of essential hypertension.¹ Garrett et al recently demonstrated that a blood pressure (BP) quantitative trait locus (QTL) exists within a newly defined 117-kb QTL region on rat chromosome 9.² By using microarray technology, the authors first found that the mRNA of Resp18 (endocrine-specific protein 18) is &7.27-fold lower in the kidney of S.R(9)x3A congenic rats (Dahl salt-resistant) than that of S rats (Dahl salt-sensitive). Furthermore, sequencing analysis revealed multiple mutations of Resp18, particularly the sequence variation (T/C) in exon 2. However, a fine-map analysis showed that Resp18 is located just outside of the 117-kb QTL region; thus, Resp18 was eliminated as a candidate gene.

The authors, however, did not address: (1) whether a homolog gene of Resp18 exists in genome, particularly in the 117-kb QTL region; (2) the significance of the Resp18 sequence variation (T/C) in exon 2; and (3) the possibilities that RESP18 plays a role in BP.

We recently demonstrated that RESP18 not only shares significant sequence similarities with the N-terminal domain (amino acid 1&200) of IA-2, a dense-core vesicle (DCV)-transmembrane protein, but also shows a similar biological function to IA-2 in terms of exocytosis of neuronal transmitter and hormones.^3,4 This means we have demonstrated that RESP18, as a DCV cargo protein, is also involved in DCV secretion (P. Yu et al, unpublished data, 2005). Furthermore, our bioinformatic analysis showed that Resp18 shares similar genomic structure and is tandemly arranged with IA-2 within . . . [Full Text of this Article]

Michael R. Garrett

Physiological Genomics Laboratory, Department of Physiology and Cardiovascular Genomics, Medical University of Ohio, Toledo, Ohio

Haijin Meng

Department of Medicine, Division of Cardiology, University of California, Los Angeles, California

John P. Rapp; Bina Joe

Physiological Genomics Laboratory, Department of Physiology and Cardiovascular Genomics, Medical University of Ohio, Toledo, Ohio