Szabo B, Hedler L, Schurr C, Starke K
Pharmakologisches Institut, Universität, Freiburg i. Br., Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1988 Oct;338(4):368-72. doi: 10.1007/BF00172111.
The effects of ACTH on the release of noradrenaline and the increase of heart rate produced by sympathetic nerve stimulation (1 Hz) were studied in isolated perfused rabbit hearts. ACTH-(1-24) 0.1-100 nmol/l increased the stimulation-evoked overflow of noradrenaline concentration-dependently, reversibly and up to two-fold. The basal outflow of noradrenaline, the basal heart rate and the stimulation-evoked increase in heart rate were not changed. Human ACTH-(1-39) also increased the evoked overflow of noradrenaline. The effect of ACTH-(1-24) 0.3 nmol/l persisted after blockade of beta-adrenoceptors with propranolol and blockade of neuronal catecholamine uptake by cocaine. ACTH-(1-24) 3 nmol/l did not change the removal of noradrenaline from the perfusion fluid, when hearts were perfused with medium containing 59 nmol/l noradrenaline. The results show that ACTH increases the action potential-evoked release of noradrenaline from cardiac postganglionic sympathetic neurones, probably by activating specific presynaptic ACTH receptors. The high potency of ACTH suggests that these presynaptic receptors may be activated in vivo by circulating ACTH under certain pathophysiological conditions.
在离体灌注兔心脏中研究了促肾上腺皮质激素（ACTH）对去甲肾上腺素释放以及交感神经刺激（1Hz）引起的心率增加的影响。0.1 - 100nmol/L的促肾上腺皮质激素（1 - 24）浓度依赖性、可逆性地增加刺激诱发的去甲肾上腺素溢出，增幅可达两倍。去甲肾上腺素的基础流出量、基础心率以及刺激诱发的心率增加均未改变。人促肾上腺皮质激素（1 - 39）也增加诱发的去甲肾上腺素溢出。在用普萘洛尔阻断β - 肾上腺素能受体并用可卡因阻断神经元儿茶酚胺摄取后，0.3nmol/L的促肾上腺皮质激素（1 - 24）的作用依然存在。当心脏用含59nmol/L去甲肾上腺素的培养基灌注时，3nmol/L的促肾上腺皮质激素（1 - 24）并未改变灌注液中去甲肾上腺素的清除。结果表明，促肾上腺皮质激素可能通过激活特定的突触前促肾上腺皮质激素受体，增加心脏节后交感神经元动作电位诱发的去甲肾上腺素释放。促肾上腺皮质激素的高效能表明，在某些病理生理条件下，这些突触前受体可能会被循环中的促肾上腺皮质激素在体内激活。
