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Sphingosine‐1‐phosphate and endothelin‐1 cause vasoconstriction of inner ear capillaries
Author(s) -
Reimann Katrin,
Scherer Elias Q.,
Wier Withrow G.,
Wangemann Philine
Publication year - 2010
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.24.1_supplement.973.12
Subject(s) - vasoconstriction , sphingosine 1 phosphate , microcirculation , cochlea , inner ear , endothelin receptor , anatomy , endothelin 1 , vasodilation , intravital microscopy , medicine , endocrinology , chemistry , microbiology and biotechnology , biology , sphingosine , receptor
Hearing depends critically on cochlear blood flow. Overproduction of sphingosine‐1‐phosphate (S1P) and endothelin (ET‐1) may be associated with sudden and immune‐mediated hearing loss. We had shown that S1P and ET‐1 are vasoconstrictors of the spiral modiolar artery, which provides the main blood supply to the cochlea (Scherer et al. 2006, 2001) and that capillaries in the lateral wall of the cochlea are contractile (Wangemann & Liu 1996). Here the goal was to determine whether S1P and ET‐1 cause a vasoconstriction of the capillaries as a down‐stream mechanism to control regional blood flow in the cochlea. Capillaries were isolated, occluded on one end, opened on the other end, and visualized in vitro by laser‐scanning microscopy. Vasoconstriction was assumed when red blood cells moved toward the open end. S1P (10 −7 to 10 −5 M) and ET‐1 (10 −10 to 10 −8 M) induced dose‐dependent vasoconstrictions. These data demonstrate the S1P and ET‐1 are vasoconstrictors in the arterial and capillary microcirculation of the inner ear. Whether overproduction of S1P and/or ET‐1 contribute to sudden and immune‐mediated hearing loss remains to be determined. NIH‐R01‐DC04280 & HL073094.