Published online before print August 31, 2009, doi: 10.1161/HYPERTENSIONAHA.109.139014
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(Hypertension. 2009;54:962.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
Yes, No, Maybe So
ENaC Proteins as Mediators of Renal Myogenic Constriction
From the Department of Physiology, University of Mississippi Medical Center, Jackson.
Correspondence to Heather A. Drummond, PhD, Associate Professor, Department of Physiology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216. E-mail hdrummond@physiology.umsmed.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The myogenic response is an intrinsic vascular response characterized by vasoconstriction in response to increases and vasodilation to decreases in perfusion pressure. Recent studies suggest this response may play a significant role in the protection of the renal microcirculation from pressure dependent injury, especially with concomitant renal disease.1 Although the myogenic response was first described more than 100 years ago, the molecular mechanisms underlying the transduction of pressure into a cellular event (ie, vasoconstriction) in vascular smooth muscle cells (VSMCs) has remained elusive. Several potential molecules with a connection to mechanosensitive responses have been identified including integrins, transient receptor potential (TRP) channels, and members of the Epithelial Na+ Channel (ENaC) family.2 Members of the ENaC family have received recent attention because of evidence for and against a role for ENaC proteins in myogenic constriction in the renal circulation. The current study by Guan et al helps to address the controversial role of ENaC in afferent arteriolar myogenic constriction.3
ENaC and closely related Acid Sensing Ion Channel (ASIC) proteins are considered potential mechanotransducers in VSMCs because of their strong evolutionary connection to a group of proteins termed degenerins. The degenerins are a group of nematode Caenorhabditis elegans proteins that comprise the ion channel pore in a large multimeric mechanosensory complex.4 Genetic evidence suggests the pore forming degenerins are tethered to the cytoskeleton and extracellular matrix and aid in force transduction.4 The extracellular matrix, linking proteins, and cytoskeletal proteins are required for proper mechanosensor channel activation.4 An analogous mechanotransducer model in mammals
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