Bloom D S, Cole A W, Palmer T N
Br J Pharmacol. 1979 Apr;65(4):587-92. doi: 10.1111/j.1476-5381.1979.tb07868.x.
1 The pressor responses to injected noradrenaline (NA) of isolated perfused femoral or renal arteries of the rabbit were studied.2 Vascular smooth muscle is relatively resistant to hypoxia. A combination of hypoxia and dinitrophenol (DNP) respiratory uncoupling was necessary to abolish the pressor response to NA. Loss of the pressor response was assumed to result from decreased capacity of arteries to form adenosine 5'-triphosphate (ATP). Reperfusion of the hypoxic arteries with oxygenated medium resulted in recovery of the pressor response to NA.3 Inclusion of inosine (10 mM) in the hypoxic perfusion medium increased significantly the rate and extent of post-hypoxic recovery of the pressor response to NA.4 Whereas the presence of inosine in the hypoxic perfusion medium aided post-hypoxic recovery, inosine had no direct action on the pressor dose response to NA. Therefore, the action of inosine was protective as opposed to direct.5 The protective action of inosine did not involve potentiation of NA binding to NA-adrenoceptor sites (the equilibrium coefficient, K(eq) for NA-receptor interaction was unaltered by hypoxia and/or inosine).6 The results are discussed in terms of a presumptive mechanism whereby inosine is believed to act by maintaining intracellular adenine nucleotide concentrations in hypoxia.
研究了家兔离体灌注股动脉或肾动脉对注射去甲肾上腺素（NA）的升压反应。
血管平滑肌对缺氧相对耐受。缺氧与二硝基苯酚（DNP）呼吸解偶联相结合对于消除对NA的升压反应是必要的。升压反应的丧失被认为是由于动脉形成三磷酸腺苷（ATP）的能力下降所致。用含氧培养基对缺氧动脉进行再灌注导致对NA的升压反应恢复。
在缺氧灌注培养基中加入肌苷（10 mM）可显著提高对NA的升压反应在缺氧后恢复的速率和程度。
虽然在缺氧灌注培养基中存在肌苷有助于缺氧后恢复，但肌苷对NA的升压剂量反应没有直接作用。因此，肌苷的作用是保护性的而非直接作用。
肌苷的保护作用不涉及增强NA与NA - 肾上腺素能受体位点的结合（NA - 受体相互作用的平衡系数K（eq）不受缺氧和/或肌苷的影响）。
根据一种推测机制对结果进行了讨论，据此认为肌苷在缺氧时通过维持细胞内腺嘌呤核苷酸浓度发挥作用。
