Volle R L, Quenzer L F
Fed Proc. 1983 Nov;42(14):3099-102.
In rat superior cervical ganglia the regulation of cyclic GMP (cGMP) formation does not involve muscarinic or adrenergic transmitters or receptors. Marked increases in cGMP content during preganglionic axonal stimulation by electric currents, elevated K+, or drugs that cause transmitter release are unaffected by muscarinic and adrenergic receptor blockade. However, the cGMP response does require Ca2+ and intact preganglionic axonal terminals. Two possibilities exist: either cGMP accumulates in the preganglionic nerves or a noncholinergic, nonadrenergic transmitter activates guanylate cyclase in postsynaptic structures. Sodium azide and nitroprusside cause cGMP accumulation in denervated ganglia, which indicates that postsynaptic structures are capable of forming cGMP. In pineal glands elevated [K+]o releases [3H]norepinephrine and causes cGMP accumulation, which suggests a relationship between the two responses and the possibility that cGMP accumulation is involved in autoinhibition of transmitter release. The finding that phentolamine, alpha-adrenergic receptor antagonists, prevent the cGMP response to K+ is compatible with this review. However, clonidine, an alpha-receptor agonist, depresses norepinephrine release but has no effect on pineal gland cGMP. Conversely, large increases in pineal gland cGMP produced by nitroprusside do not affect K+-evoked norepinephrine release. For these reasons it is not possible to relate cGMP to the auto-inhibition of [3H]norepinephrine release that is mediated by prejunctional alpha-adrenergic receptors.
在大鼠颈上神经节中，环磷酸鸟苷（cGMP）生成的调节不涉及毒蕈碱或肾上腺素能递质或受体。在通过电流、高钾或引起递质释放的药物进行节前轴突刺激期间，cGMP含量的显著增加不受毒蕈碱和肾上腺素能受体阻断的影响。然而，cGMP反应确实需要钙离子和完整的节前轴突终末。存在两种可能性：要么cGMP在节前神经中积累，要么一种非胆碱能、非肾上腺素能递质激活突触后结构中的鸟苷酸环化酶。叠氮化钠和硝普钠可使去神经节中的cGMP积累，这表明突触后结构能够形成cGMP。在松果体中，细胞外高钾浓度升高会释放[3H]去甲肾上腺素并导致cGMP积累，这表明这两种反应之间存在关联，并且cGMP积累可能参与递质释放的自身抑制。酚妥拉明（一种α-肾上腺素能受体拮抗剂）可阻止cGMP对钾离子的反应，这一发现与本综述一致。然而，可乐定（一种α-受体激动剂）可抑制去甲肾上腺素释放，但对松果体cGMP没有影响。相反，硝普钠引起的松果体cGMP大幅增加并不影响钾离子诱发的去甲肾上腺素释放。由于这些原因，无法将cGMP与由节前α-肾上腺素能受体介导的[3H]去甲肾上腺素释放的自身抑制联系起来。
