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Purpose: Fentanyl was reported to inhibit the α1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the α1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta. Materials and Methods: Aortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3×10-7, 10-6, 3×10-6 M), 5- methylurapidil (3×10-8, 10-7, 3×10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3×10-9, 10-8, 3×10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3×10-9 M prazosin, 10-9 M 5-methylurapidil or 3×10-9 M BMY 7378. Results: Fentanyl (10-6, 3×10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5- methylurapidil and BMY 7378 were estimated to be 7.71 ± 0.15 and 8.99 ± 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3×10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 ± 2.3% reduction in phenylephrine-induced maximal contraction. Conclusion: The results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the α1D-adrenoceptormediated contraction of the rat aorta.
Purpose: Fentanyl was reported to inhibit the α1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the α1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta. Materials and Methods: Aortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3×10-7, 10-6, 3×10-6 M), 5- methylurapidil (3×10-8, 10-7, 3×10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3×10-9, 10-8, 3×10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3×10-9 M prazosin, 10-9 M 5-methylurapidil or 3×10-9 M BMY 7378. Results: Fentanyl (10-6, 3×10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5- methylurapidil and BMY 7378 were estimated to be 7.71 ± 0.15 and 8.99 ± 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3×10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 ± 2.3% reduction in phenylephrine-induced maximal contraction. Conclusion: The results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the α1D-adrenoceptormediated contraction of the rat aorta.
