Endothelin-1 causes luminal constrictions in rat cochlear veins

Serum levels of the vasoconstrictor Endothelin-1 (ET-1) increase in ischemia and systemic hypertension. We examined the effects of ET- I on the cochlear microvasculature. Blood vessels were cast with methacrylate in adult male Wistar Kyoto rats, 10 min after intravenous injection of ET-1 (1.0 μg/kg)...

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Published inHearing research Vol. 112; no. 1; pp. 33 - 43
Main Authors Franz, Peter, Aharinejad, Seyedhossein, Miksovsky, Aurelia, Schraufnagel, Dean E., Larson, Erik K., Marks, Sandy C.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.10.1997
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Summary:Serum levels of the vasoconstrictor Endothelin-1 (ET-1) increase in ischemia and systemic hypertension. We examined the effects of ET- I on the cochlear microvasculature. Blood vessels were cast with methacrylate in adult male Wistar Kyoto rats, 10 min after intravenous injection of ET-1 (1.0 μg/kg); control animals received saline. Systemic blood pressure was recorded continuously. ET-1 increased the average systolic pressure by 18% and average diastolic pressure by 22% ( P < 0.01). Scanning electron microscopy of cast vessels showed multiple circumscribed luminal constrictions on: (1) postcapillary venules; (2) collecting veins; (3) where collecting veins merged with the spiral modiolar vein; (4) on the spiral modiolar vein itself. Circumscribed constrictions in arteries were not observed. In ET-1 injected animals focal contractions of collecting veins reduced luminal width by 13.4% ± 2.9 ( P < 0.01). In control rats, constrictions on venous casts were minimal and constrictions on arteries were not observed. The present study shows that ET-1 is involved in local control of cochlear blood flow in that it focally contracts cochlear veins. It is suggested that this might be due to the high affinity of ET-1 receptors and/or the large number of ET-1 receptors on contractile cells in venous walls.
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ISSN:0378-5955
1878-5891
DOI:10.1016/S0378-5955(97)00112-3