Endothelin (1 nM-0.3 microM) produced a concentration-related contraction of mucosa-free muscle strips excised from the dome of the human urinary bladder. The response to endothelin was unaffected by either atropine (1 microM) or nifedipine (1 microM) at concentrations that abolished the response to carbachol and KCl, respectively. These findings indicate that mechanisms other than activation of dihydropyridine- and voltage-sensitive calcium channels may be involved in the action of endothelin on smooth muscles.
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Maggi et al. (1989) studied this question.
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