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 in | Hearing research Vol. 112; no. 1; pp. 33 - 43 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.10.1997
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Subjects | |
Online Access | Get full text |
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0378-5955 1878-5891 |
DOI: | 10.1016/S0378-5955(97)00112-3 |