Giacomini V A, Reis C C
Gen Pharmacol. 1986;17(2):219-25. doi: 10.1016/0306-3623(86)90142-4.
Norepinephrine (NE) and histamine (His) cause a dose related increase in the rate of the guinea pig isolated right atria. The rate increase induced by both amines has been shown to be mediated by pharmacologically different receptors. His shifted the NE CEC to the right in a non parallel fashion. Cimetidine (10(-4) mol/l) abolished this antagonism. Norepinephrine (3 X 10(-7) mol/l) shifted to the right the His CEC also in a non parallel fashion. Practolol (10(-4) mol/l) abolished this antagonism. Theophylline (10(-4) mol/l) reverted both: the antagonistic action of His related to the NE chronotropic effect and the antagonistic action of NE related to the His chronotropic effect. The reversal of the antagonism could be the result of the block of purinergic P1-receptors by theophylline. This block impairs the chronotropic effect of adenilic compounds which can function as a modulater of cardiac rate through a negative feed back mechanism.
去甲肾上腺素(NE)和组胺(His)可使豚鼠离体右心房的速率呈剂量依赖性增加。已证明这两种胺类引起的速率增加是由药理学上不同的受体介导的。His以非平行方式使NE的累积浓度效应曲线(CEC)右移。西咪替丁(10⁻⁴mol/L)消除了这种拮抗作用。去甲肾上腺素(3×10⁻⁷mol/L)也以非平行方式使His的CEC右移。心得宁(10⁻⁴mol/L)消除了这种拮抗作用。茶碱(10⁻⁴mol/L)逆转了两者:His对NE变时效应的拮抗作用以及NE对His变时效应的拮抗作用。拮抗作用的逆转可能是由于茶碱阻断了嘌呤能P1受体。这种阻断损害了腺苷酸化合物的变时效应,腺苷酸化合物可通过负反馈机制作为心率调节剂发挥作用。