Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2006
[Vasorelaxant effect of sulfur dioxide derivatives on isolated aortic rings of rats and its mechanisms].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Du Shu-xu, Zhang Chun-yu, Jin Hong-fang, Du Jun-bao, Tang Chao-shu
Аннотация
OBJECTIVE: To investigate the vasorelaxant effect of sulfur dioxide (SO(2)) on isolated aortic rings of rats in vitro and its relaxation mechanisms.
METHODS: We perffused the isolated aortic rings of rats, and precontracted the rings with noradrenaline (NE), then observed the relaxant reactivity of SO(2) derivatives, mixture of sulfite and hydrogen sulfite [Na(2)SO(3)/NaHSO(3) 3:1(amount of substance)], to the aortic rings. Meanwhile, we studied the influence of glibenclamide and nicardipine, blockers of K(ATP) and L-calcium channels, on the vasorelaxant reactivity of SO(2) derivatives. We further incubated the aortic rings with hydroxamate (HDX), the inhibitor of SO(2) endogenous generating enzymes, and SO(2) derivatives (4 mmol/L) in vitro, then observed the contraction of the aortic rings to NE.
RESULTS: Isolated aortic rings of rats exhibited relaxant reactivity to Na(2)SO(3)/NaHSO(3) (0-12 mmol/L) in a concentration-dependent manner. IC(50) of the relaxation curve was (7.28+/-0.12) mmol/Lìand Emax was 78.79%+/-3.24%. Glibenclamide (1x10(-6) mol/L) inhibited the vasorelaxation to low dose Na(2)SO(3)/NaHSO(3) (<or=4 mmol/L), whereas it failed to inhibit the vasorelaxation to high dose of Na(2)SO(3)/NaHSO(3) (>6 mmol/L). Nicardipine (1x10(-9) mol/L) could decrease the contraction of the rings to NE, and even could inhibit the relaxation of Na(2)SO(3)/NaHSO(3) almost completely. The inhibition of the endogenous SO(2) production with HDX (1x10(-4) mol/L), resulted in an increase in the contraction of rings. The contraction curve to NE shifted to the left, and IC(50) also changed from (6.48+/-0.84)x10(-7) mol/L to (3.97+/-1.63)x10(-7) mol/L (P<0.01). However, after the incubation of aortic rings with Na(2)SO(3)/NaHSO(3) (4 mmol/L), the contraction curve to NE shifted to the right, and IC(50) changed from (6.48+/-0.84)x10(-7) mol/L to (4.93+/-0.81)x10(-5) mol/L (P<0.01).
CONCLUSION: SO(2) could relax vascular smooth muscles, and the mechanism might be associated with calcium channels and K(ATP) channels, suggesting that endogenous SO(2) could modulate the cardiovascular function.
METHODS: We perffused the isolated aortic rings of rats, and precontracted the rings with noradrenaline (NE), then observed the relaxant reactivity of SO(2) derivatives, mixture of sulfite and hydrogen sulfite [Na(2)SO(3)/NaHSO(3) 3:1(amount of substance)], to the aortic rings. Meanwhile, we studied the influence of glibenclamide and nicardipine, blockers of K(ATP) and L-calcium channels, on the vasorelaxant reactivity of SO(2) derivatives. We further incubated the aortic rings with hydroxamate (HDX), the inhibitor of SO(2) endogenous generating enzymes, and SO(2) derivatives (4 mmol/L) in vitro, then observed the contraction of the aortic rings to NE.
RESULTS: Isolated aortic rings of rats exhibited relaxant reactivity to Na(2)SO(3)/NaHSO(3) (0-12 mmol/L) in a concentration-dependent manner. IC(50) of the relaxation curve was (7.28+/-0.12) mmol/Lìand Emax was 78.79%+/-3.24%. Glibenclamide (1x10(-6) mol/L) inhibited the vasorelaxation to low dose Na(2)SO(3)/NaHSO(3) (<or=4 mmol/L), whereas it failed to inhibit the vasorelaxation to high dose of Na(2)SO(3)/NaHSO(3) (>6 mmol/L). Nicardipine (1x10(-9) mol/L) could decrease the contraction of the rings to NE, and even could inhibit the relaxation of Na(2)SO(3)/NaHSO(3) almost completely. The inhibition of the endogenous SO(2) production with HDX (1x10(-4) mol/L), resulted in an increase in the contraction of rings. The contraction curve to NE shifted to the left, and IC(50) also changed from (6.48+/-0.84)x10(-7) mol/L to (3.97+/-1.63)x10(-7) mol/L (P<0.01). However, after the incubation of aortic rings with Na(2)SO(3)/NaHSO(3) (4 mmol/L), the contraction curve to NE shifted to the right, and IC(50) changed from (6.48+/-0.84)x10(-7) mol/L to (4.93+/-0.81)x10(-5) mol/L (P<0.01).
CONCLUSION: SO(2) could relax vascular smooth muscles, and the mechanism might be associated with calcium channels and K(ATP) channels, suggesting that endogenous SO(2) could modulate the cardiovascular function.