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Impaired pressure-induced constriction in mouse middle cerebral arteries of ASIC2 knockout mice

¹Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi; and ²Department of Cellular Biology and Physiology, University of New Mexico Health Science Center, Albuquerque, New Mexico

Submitted 29 November 2007 ; accepted in final form 6 February 2008

Recent studies from our laboratory demonstrated the importance of mechanosensitive epithelial Na⁺ channel (ENaC) proteins in pressure-induced constriction in renal and cerebral arteries. ENaC proteins are closely related to acid-sensing ion channel 2 (ASIC2), a protein known to be required for normal mechanotransduction in certain sensory neurons. However, the role of the ASIC2 protein in pressure-induced constriction has never been addressed. The goal of the current study was to investigate the role of ASIC2 proteins in pressure-induced, or myogenic, constriction in the mouse middle cerebral arteries (MCAs) from ASIC2 wild-type (+/+), heterozygous (+/–), and null (–/–) mice. Constrictor responses to KCl (20–80 mM) and phenylephrine (10^–7–10^–4 M) were not different among groups. However, vasoconstrictor responses to increases in intraluminal pressure (15–90 mmHg) were impaired in MCAs from ASIC2^–/– and ^+/– mice. At 60 and 90 mmHg, MCAs from ASIC2^+/+ mice generated 13.7 ± 2.1% and 15.8 ± 2.0% tone and ASIC2^–/– mice generated 7.4 ± 2.8% and 12.5 ± 2.4% tone, respectively. Surprisingly, MCAs from ASIC2^+/– mice generated 1.2 ± 2.2% and 3.9 ± 1.8% tone at 60 and 90 mmHg. The reason underlying the total loss of myogenic tone in the ASIC2^+/– is not clear, although the loss of mechanosensitive β- and -ENaC proteins may be a contributing factor. These results demonstrate that normal ASIC2 expression is required for normal pressure-induced constriction in the MCA. Furthermore, ASIC2 may be involved in establishing the basal level of myogenic tone.

mechanotransduction; myogenic constriction; degenerin; acid-sensing ion channel

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