Bone E A, Fretten P, Palmer S, Kirk C J, Michell R H
Biochem J. 1984 Aug 1;221(3):803-11. doi: 10.1042/bj2210803.
An accumulation of 3H-labelled inositol phosphates is observed when prelabelled rat superior cervical sympathetic ganglia are exposed to [8-arginine]vasopressin or to muscarinic cholinergic stimuli. The response to vasopressin is much greater than the response to cholinergic stimuli. The response to vasopressin is blocked by a V1-vasopressin antagonist, and oxytocin is a much less potent agonist than vasopressin. Vasopressin causes no increase in the cyclic AMP content of ganglia. These ganglia therefore appear to have functional V1-vasopressin receptors that are capable of activating inositol lipid breakdown, but no V2-receptors coupled to adenylate cyclase. The first [3H]inositol-labelled products to accumulate in stimulated ganglia are inositol trisphosphate and inositol bisphosphate, suggesting that the initiating reaction in stimulated inositol lipid metabolism is a phosphodiesterase-catalysed hydrolysis of phosphatidylinositol 4,5-bisphosphate (and possibly also phosphatidylinositol 4-phosphate). This response to exogenous vasopressin occurs in ganglia incubated in media of reduced Ca2+ concentration. The physiological functions of the V1-vasopressin receptors of these ganglia remain unknown.
当预先标记的大鼠颈上神经节暴露于[8-精氨酸]加压素或毒蕈碱胆碱能刺激时，可观察到3H标记的肌醇磷酸酯的积累。对加压素的反应远大于对胆碱能刺激的反应。对加压素的反应被V1加压素拮抗剂阻断，且催产素作为激动剂的效力远低于加压素。加压素不会使神经节中的环磷酸腺苷含量增加。因此，这些神经节似乎具有能够激活肌醇脂质分解的功能性V1加压素受体，但没有与腺苷酸环化酶偶联的V2受体。在受刺激的神经节中首先积累的[3H]肌醇标记产物是肌醇三磷酸和肌醇二磷酸，这表明受刺激的肌醇脂质代谢中的起始反应是磷酸二酯酶催化的磷脂酰肌醇4,5-二磷酸（可能还有磷脂酰肌醇4-磷酸）的水解。这种对外源加压素的反应发生在低钙浓度培养基中孵育的神经节中。这些神经节中V1加压素受体的生理功能仍然未知。
