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(Hypertension. 2004;44:616.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Sensing Tension

Recognizing ENaC as a Stretch Sensor

From the University of Alabama, Birmingham.

Correspondence to Dale J. Benos, Department of Physiology and Biophysics, University of Alabama-Birmingham, 1918 University Blvd, 706 BHSB, Birmingham, AL 35294-0005, E-mail benos@physiology.uab.edu

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

Homeostasis demands the integration and processing of a myriad of different input signals from a variety of sources. Regulation of central blood pressure is one such homeostatic system that depends critically on both volumetric and hemodynamic information. A common element for cardiovascular data transfer is sensing mechanical alterations such as cellular volume changes, changes in shear stresses, or changes in membrane tension or curvature. Stretch activation of membrane proteins, specifically ion channels, transduces hydrostatic pressure differences in the major blood vessels (via aortic and carotid baroreceptors) and small arteries and arterioles (via vascular smooth muscle cells [VSMCs]). Electrical signals from the baroreceptors travel via afferent nerves to integrative centers in the brain for processing, and appropriate efferent signals are generated to alter heart rate and peripheral resistance in a classic negative feedback loop. In contrast, there are important local autoregulatory control mechanisms that exist to alter blood flow in the capillary beds of the kidney, musculature, intestine, heart, and brain. These local effectors are also under central control to adjust peripheral vascular resistance when necessary. Presumptive mechanosensitive ion channels in VSMCs lining the arterioles are thought to subserve this function.

Until now, the identity of VSMC mechanosensitive channels was left to one’s musings. Wu and Davis¹ reported a stretch-activated cation current in porcine coronary VSMCs. This current was blocked by hexamethylamiloride and Grammostolla spatulata venom, both of which are thought to block mechanosensitive channels.^1–3 Golestaneh et al⁴ established that amiloride-sensitive, epithelial Na⁺ channels (ENaCs) were expressed in a vascular endothelial . . . [Full Text of this Article]

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