Abstract
Abstract: :
Purpose: To investigate whether unoprostone (the active compound of Rescula®) can antagonize a contraction induced by endothelin-1 in isolated porcine ciliary arteries. Methods: Changes in the vascular tension were measured with a myograph system (isometric force measurement) and expressed in percent of contractions induced by 100 mM potassium chloride (mean ± standard error). Quiescent or endothelin-1-precontracted (10 nM) vessels were exposed, in a cumulative manner, to increasing concentrations of unoprostone (0.1 nM to 0.1 mM). Time-control experiments were conducted in parallel without unoprostone. Results: Unoprostone induced a vasoconstriction in quiescent vessels at concentrations of 1 µM and above (maximum: 43 ± 4 %, n = 5, P < 0.05 versus time-control). In endothelin-1-precontracted vessels not exposed to unoprostone (time-control) a spontaneous loss of tension could be observed over time (maximum: -24 ± 6%, n = 7). In comparison to the tension measured in time-control experiments, unoprostone induced contractions that became significant at concentrations higher than 1 µM (maximum: 23 ± 6%; n = 7, P < 0.001). At the highest concentration of unoprostone tested (0.1 mM), the vascular tension measured was about 47% higher than the one in time-control experiments. Conclusion: The results of the present in vitro pharmacological study (on the basis of which in principle no clinical interpretation should be made) indicate that, at least in isolated porcine ciliary arteries, unoprostone is a vasoconstrictor that is unable to antagonize a precontraction evoked by endothelin-1.