Abstract
The tension developed by rat aortic strips in response to endothelin-1 is determined by three types of mechanisms: a [Ca 2+]o independent mechanism, L-type Ca 2+ channels and a [Ca 2+]o dependent, verapamil insensitive, mechanism. Their relative contributions to the tension recorded 30 minutes after the addition of 50 nM endothelin-1 were 43%, 34% and 23%. Upon longer exposures to endothelin-1, the whole tension could be abolished by reducing [Ca 2+]o to 20 nM. Endothelin-1 induced contractions were highly sensitive to changes in free [Ca 2+]o. The EC50 value for the [Ca 2+]o dependence of endothelin-1 induced contractions was 600 nM, a value 400 times lower than the corresponding value found for KCl induced contractions (250 μM). These results suggest that extracellular Ca 2+ is necessary for full tension development in response to endothelin-1 but that a major action of endothelin-1 is to increase the sensitivity of pharmacomechanical coupling mechanisms to Ca 2+.
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