Berggren A, Dahlström A, Rubenson A, Sillén U
Department of Pediatric Surgery, Ostra Hospital, Gothenburg, Sweden.
J Neural Transm Gen Sect. 1992;90(1):33-44. doi: 10.1007/BF01250516.
Muscle strips from rat and human detrusor were studied using indirect immunofluorescence and electrical nerve stimulation in an organ bath. Immunoreactivity towards dynorphin was observed in varicose nerve fibres in the detrusor muscle and around immunonegative nerve cell bodies in the prevesical ganglia of the rat. In vitro, dynorphin A (1-13) (10(-13)-10(-6) M) strongly facilitated detrusor contraction induced by electrical field stimulation (EFS). This facilitation was counteracted by morphine (10(-10) and 10(-8) M) and naloxone (10(-10) and 10(-8) M) in a competitive manner. The facilitation could also be counteracted by the addition of the kappa-receptor antagonist M(r) 2266 (10(-7) M). Muscarinic blockade, achieved with atropine (10(-6) M), did not alter the effect of dynorphin A (1-13). Addition of phentolamine mesylate (10(-6) M), and propranolol (10(-6) M) per se facilitated the EFS-induced contractions. Both adrenergic blockade as well as the addition of the substance P blocker spantide, counteracted the facilitating effect of dynorphin A (1-13).
Dynorphin A immunoreactive material was found to be present in nerves in the rat detrusor and in prevesical ganglia. Dynorphin A (1-13) facilitated the detrusor contraction, possibly via actions on kappa-opioid receptors and interaction with non-cholinergic nerves.
在器官浴槽中，使用间接免疫荧光和电神经刺激研究了大鼠和人逼尿肌的肌条。在大鼠逼尿肌的曲张神经纤维和膀胱前神经节中免疫阴性神经细胞体周围观察到对强啡肽的免疫反应性。在体外，强啡肽A（1-13）（10⁻¹³ - 10⁻⁶ M）强烈促进电场刺激（EFS）诱导的逼尿肌收缩。这种促进作用被吗啡（10⁻¹⁰和10⁻⁸ M）和纳洛酮（10⁻¹⁰和10⁻⁸ M）以竞争性方式抵消。添加κ-受体拮抗剂M(r) 2266（10⁻⁷ M）也可抵消这种促进作用。用阿托品（10⁻⁶ M）实现的毒蕈碱阻断并未改变强啡肽A（1-13）的作用。添加甲磺酸酚妥拉明（10⁻⁶ M）和普萘洛尔（10⁻⁶ M）本身促进了EFS诱导的收缩。肾上腺素能阻断以及添加P物质阻断剂spantide均抵消了强啡肽A（1-13）的促进作用。
发现强啡肽A免疫反应性物质存在于大鼠逼尿肌和膀胱前神经节的神经中。强啡肽A（1-13）促进逼尿肌收缩，可能是通过作用于κ-阿片受体并与非胆碱能神经相互作用。
