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Maintained intracellular acidification reduces myogenic tone and vasomotion in mice cerebral arteries (1098.3)
Author(s) -
Aalkjaer Christian,
Thomsen Axel,
Kim Sukhan,
Aalbaek Filip,
Boedtkjer Ebbe
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1098.3
Subject(s) - cerebral arteries , vasomotion , intracellular ph , medicine , knockout mouse , vascular smooth muscle , myogenic contraction , endocrinology , chemistry , biology , extracellular , vasodilation , biochemistry , receptor , smooth muscle
The effect of smooth muscle (VSMC) and endothelial cell pH (pH i ) on myogenic tone is unknown. Here the role of Na + ,HCO 3 ‐ ‐cotransporter NBCn1 for pH i in these cells, and the influence of low pH i on myogenic tone and vasomotion were determined in intact mouse middle cerebral arteries. Na + ,HCO 3 ‐ ‐cotransport contributed to extrusion of acid from wildtype arteries but not from arteries where NBCn1 was knocked out. pH i of VSMCs was approximately 0.3 units lower in arteries from NBCn1 knockout than wildtype mice. Substantial myogenic tone developed after inhibition of NO‐synthase with L‐NAME in wildtype arteries. Less tone developed in arteries from NBCn1 knockout mice. This myogenic tone was in both type of arteries abolished by the rho‐kinase inhibitor Y‐27632. The arteries displayed vasomotion, which was attenuated in arteries from NBCn1 knockout mice. No differences in membrane potential or [Ca 2+ ] i were seen between VSMC in arteries from NBCn1 knockout and wildtype mice. We propose that NO production and rho‐kinase‐dependent VSMC Ca 2+ ‐sensitivity are reduced at low pH i in mouse middle cerebral arteries, which likely impedes the ability of these arteries to adjust to changes in perfusion pressure.