Loutzenhiser and Aaronson1 argue that a lack of effect of amiloride and benzamil at 1 μmol/L suggests that “[epithelial sodium channels] ENaC plays little if any role in myogenic signaling” in the afferent arteriole. They are correct. However, we do not hypothesize that the classical “ENaC channel” (formed by αβγENaC) is acting as a vascular mechanosensor.1 We hypothesize the proteins that form ENaC channels (ie, βENaC and γENaC) in epithelial cells associate with related acid-sensing ion channel (ASIC) proteins to form a mechanosensor,2 a very important distinction. We have use the Caenorhabditis elegans mechanosensor as a model for a mammalian …
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