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Decreased expression of NCX impairs arteriolar myogenic constriction
Author(s) -
Raina Hema,
Hill Michael
Publication year - 2007
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.21.6.a1235-d
Subject(s) - depolarization , vasoconstriction , myogenic contraction , chemistry , extracellular , sodium calcium exchanger , membrane potential , vascular smooth muscle , myocyte , medicine , intracellular , microbiology and biotechnology , biophysics , endocrinology , biochemistry , biology , smooth muscle
Arteriolar myogenic vasoconstriction occurs when stretch or increased membrane tension leads to smooth muscle cell (SMC) depolarization and opening of voltage‐gated Ca2+ channels. While the mechanism underlying the depolarization is uncertain a role for non‐selective cation channels has been suggested. As such channels may be expected to pass Na+ we hypothesized that reverse mode Na+Ca2+ exchange (NCX) may act to remove Na+ and hence play a role in myogenic signaling. Further, reverse mode function of the NCX is favored by the membrane potential found in myogenically active arterioles. All experiments were performed on isolated rat skeletal muscle arterioles (passive diameter ~150um). Reduction of extracellular Na+ to promote reverse‐mode NCX activity caused vasoconstriction and increased intracellular Ca2+. Western blotting confirmed the existence of NCX protein while real‐time PCR studies demonstrated that the major isoform expressed was NCX1. Oligonucleotide knockdown (24 and 36 hrs) of NCX inhibited the vasoconstrictor response to reduced extracellular Na+ while also impairing both steady‐state myogenic responses (as shown by pressure‐diameter relationships) and acute reactivity to a 50 to 120mmHg pressure step. The data are consistent with reverse mode activity of the NCX in arterioles and a contribution of this exchanger to myogenic vasoconstriction.