Turner A J, Seale J P, Black J L, Compton M R, Shaw J
Naunyn Schmiedebergs Arch Pharmacol. 1987 Mar;335(3):269-73. doi: 10.1007/BF00172795.
Contractile responses of guinea-pig peripheral lung strips to noradrenaline were determined in the presence of propranolol (2.5 X 10(-6) mol/l). All strips (n = 44) contracted to noradrenaline and a geometric mean EC50 of 1.4 X 10(-6) mol/l (1.1 X 10(-6) mol/l, 1.8 X 10(-6) mol/l 95% confidence limits) was obtained. Contractions were antagonised by phentolamine (5 X 10(-7)-10(-5) mol/l) and by prazosin (10(-8)-10(-7) mol/l). Dose-ratios (DR) were calculated and log (DR-1) was plotted against log concentration of antagonist to yield slopes (+/- SE) of 0.84 +/- 0.14 and 0.73 +/- 0.22 respectively which were not significantly different from unity. A pA2 value (+/- SE) of 6.7 +/- 0.2 was obtained for phentolamine and 7.5 +/- 0.1 for prazosin. Yohimbine (10(-7)-10(-5) mol/l) did not significantly affect the maximal tension generated or the EC50 values for noradrenaline. These results suggest that alpha 1 adrenoceptors are mediating the contractile responses to noradrenaline. In the presence of cocaine (10(-5) mol/l, n = 18), normetanephrine (2 X 10(-5) mol/l, n = 15), hydrocortisone (2.5 X 10(-5) mol/l, n = 15) and normetanephrine (2 X 10(-5) mol/l) plus cocaine (10(-5) mol/l, n = 15) pA2 values for phentolamine of 6.9, 6.7, 6.6, and 6.3 respectively were obtained. Since these pA2 values are not significantly different from 6.7, it is unlikely that this original pA2 value, which is lower than values obtained with phentolamine at alpha-adrenoceptors in other tissues, may be explained by neuronal or extraneuronal uptake of noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
在普萘洛尔(2.5×10⁻⁶摩尔/升)存在的情况下,测定了豚鼠外周肺条对去甲肾上腺素的收缩反应。所有肺条(n = 44)对去甲肾上腺素均产生收缩反应,得到的几何平均EC50为1.4×10⁻⁶摩尔/升(1.1×10⁻⁶摩尔/升,1.8×10⁻⁶摩尔/升,95%置信区间)。酚妥拉明(5×10⁻⁷ - 10⁻⁵摩尔/升)和哌唑嗪(10⁻⁸ - 10⁻⁷摩尔/升)可拮抗收缩反应。计算了剂量比(DR),并将log(DR - 1)对拮抗剂浓度的对数作图,得到斜率(±标准误)分别为0.84±0.14和0.73±0.22,与1无显著差异。酚妥拉明的pA2值(±标准误)为6.7±0.2,哌唑嗪的为7.5±0.1。育亨宾(10⁻⁷ - 10⁻⁵摩尔/升)对去甲肾上腺素产生的最大张力或EC50值无显著影响。这些结果表明,α1肾上腺素能受体介导了对去甲肾上腺素的收缩反应。在可卡因(10⁻⁵摩尔/升,n = 18)、去甲变肾上腺素(2×10⁻⁵摩尔/升,n = 15)、氢化可的松(2.5×10⁻⁵摩尔/升,n = 15)以及去甲变肾上腺素(2×10⁻⁵摩尔/升)加可卡因(10⁻⁵摩尔/升,n = 15)存在的情况下,酚妥拉明的pA2值分别为6.9、6.7、6.6和6.3。由于这些pA2值与6.7无显著差异,所以最初这个低于在其他组织中α - 肾上腺素能受体上用酚妥拉明获得的值的pA2值,不太可能用去甲肾上腺素的神经元或非神经元摄取来解释。(摘要截短至250字)