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Background  Vasospasm of the spiral modiolar artery (SMA) may cause ischemic stroke of the inner ear. Endothelin-1 (ET-1) induces a strong, long-lasting constriction of the SMA by increasing contractile apparatus Ca 2+  sensitivity via Rho-kinase. We therefore tested several Rho-kinase inhibitors and a cell-permeable analogue of cAMP (dbcAMP) for their ability to reverse ET-1-induced constriction and Ca 2+ -sensitization.    Methods  The present study employed SMA isolated from gerbil temporal bones. Ca 2+ sensitivity was evaluated by correlating vascular diameter and smooth muscle cell [Ca 2+ ] i , measured by fluo-4-microfluorometry and videomicroscopy.    Results  The Rho-kinase inhibitors Y-27632, fasudil, and hydroxy-fasudil reversed ET-1-induced vasoconstriction with an  IC 50   of 3, 15, and 111 μmol/L, respectively. DbcAMP stimulated a dose-dependent vasodilation ( Ec 50   = 1 mmol/L) and a reduction of [Ca 2+ ] i  ( EC 50   = 0.3 μmol/L) of ET-1-preconstricted vessels (1 nmol/L). Fasudil and dbcAMP both reversed the ET-1-induced increase in Ca 2+  sensitivity.    Conclusion  Rho-kinase inhibition and dbcAMP reversed ET-1-induced vasoconstriction and Ca 2+ -sensitization. Therefore, Rho-kinase inhibitors or cAMP modulators could possess promise as pharmacological tools for the treatment of ET-1-induced constriction, ischemic stroke and sudden hearing loss.

bmc ear, nose and throat disorders

Pharmacological reversal of endothelin-1 mediated constriction of the spiral modiolar artery: a potential new treatment for sudden sensorineural hearing loss