BACKGROUND: To assess if the vasorelaxing properties of the ocular hypotensive beta-blocker carteolol could share some pharmacological features of calcium-channel antagonists in isolated porcine ciliary arteries. METHODS: In a myograph system (isometric force measurement), quiescent vessels were contracted with increasing concentrations of potassium chloride (KCl: 4.7 - 30 mM) in the presence of different concentrations of extracellular calcium (Ca (++): 0 - 10 mM) and/or carteolol (0 - 1 mM). Vessels precontracted with 20 mM KCl were exposed (cumulative manner) to carteolol (0.03 - 3 mM) in the presence of different concentrations of Ca (++) (0.25, 2.5, 10 mM). Contractions and relaxations are expressed in percent of 100 mM and 20 mM KCl-induced contractions, respectively (mean +/- SEM). RESULTS: Contractions induced by 30 mM KCl (99.0 +/- 4.8 %) were abolished in the absence of Ca (++) and markedly inhibited in the presence of carteolol (1 mM: 40.6 +/- 4.0 %). The inhibitory effect of carteolol on KCl-induced contractions was potentiated (0.25 mM: 6 +/- 2 %) by decreasing and reversed (10 mM: 94 +/- 5 %) by increasing Ca (++) concentrations. Vessels precontracted with KCl were relaxed by carteolol (maximum: 82 +/- 9 %), an effect potentiated (102 +/- 10 %) by lowering or inhibited (27 +/- 11 %) by increasing Ca (++) concentrations. DISCUSSION: The present in vitro pharmacological study, for which in principle no clinical interpretation should be made, suggests that carteolol shares, at rather high concentrations, some characteristics that apparently could mimic certain effects of calcium-channel blockers.
BACKGROUND: To assess if the vasorelaxing properties of the ocular hypotensive beta-blockercarteolol could share some pharmacological features of calcium-channel antagonists in isolated porcine ciliary arteries. METHODS: In a myograph system (isometric force measurement), quiescent vessels were contracted with increasing concentrations of potassium chloride (KCl: 4.7 - 30 mM) in the presence of different concentrations of extracellular calcium (Ca (++): 0 - 10 mM) and/or carteolol (0 - 1 mM). Vessels precontracted with 20 mM KCl were exposed (cumulative manner) to carteolol (0.03 - 3 mM) in the presence of different concentrations of Ca (++) (0.25, 2.5, 10 mM). Contractions and relaxations are expressed in percent of 100 mM and 20 mM KCl-induced contractions, respectively (mean +/- SEM). RESULTS: Contractions induced by 30 mM KCl (99.0 +/- 4.8 %) were abolished in the absence of Ca (++) and markedly inhibited in the presence of carteolol (1 mM: 40.6 +/- 4.0 %). The inhibitory effect of carteolol on KCl-induced contractions was potentiated (0.25 mM: 6 +/- 2 %) by decreasing and reversed (10 mM: 94 +/- 5 %) by increasing Ca (++) concentrations. Vessels precontracted with KCl were relaxed by carteolol (maximum: 82 +/- 9 %), an effect potentiated (102 +/- 10 %) by lowering or inhibited (27 +/- 11 %) by increasing Ca (++) concentrations. DISCUSSION: The present in vitro pharmacological study, for which in principle no clinical interpretation should be made, suggests that carteolol shares, at rather high concentrations, some characteristics that apparently could mimic certain effects of calcium-channel blockers.