Smooth Muscle Research Centre, Dundalk Institute of Technology, Dundalk, Ireland.
J Urol. 2011 Aug;186(2):745-52. doi: 10.1016/j.juro.2011.03.140. Epub 2011 Jun 17.
Adenosine triphosphate is capable of relaxing and contracting urethral smooth muscle. The mechanisms responsible for the relaxing effects of adenosine triphosphate have been well studied but those involved in the contractile response are still unclear. We investigated the contributions of interstitial cells of Cajal and smooth muscle cells to nerve mediated, adenosine triphosphate dependent contractions of urethral smooth muscle.
Tension recordings were made from strips of rabbit urethral smooth muscle. Recordings were made of membrane potential and ionic currents from freshly isolated smooth muscle cells and interstitial cells of Cajal using the patch clamp technique.
Stimulating intramural nerves in urethral smooth muscle yielded contractions that were inhibited by the broad spectrum P2 receptor inhibitor pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate and the P2X receptor agonist α,β-methylene adenosine triphosphate but not by the P2Y receptor antagonist MRS2500. When studied under voltage clamp at a holding potential of -60 mV, interstitial cells of Cajal showed spontaneous transient inward currents that were increased in frequency by adenosine triphosphate but not by α,β-methylene adenosine triphosphate. In contrast, smooth muscle cells were quiescent but responded to adenosine triphosphate and α,β-methylene adenosine triphosphate by producing a single transient inward current. Currents evoked by adenosine triphosphate in smooth muscle cells were inhibited by α,β-methylene adenosine triphosphate, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate and suramin, and by a decrease in extracellular Na+ from 130 to 13 mM.
Stimulating purinergic nerves in rabbit urethral smooth muscle induces contractions via the activation of P2X receptors on smooth muscle cells.
三磷酸腺苷能够舒张和收缩尿道平滑肌。三磷酸腺苷舒张作用的机制已经得到了很好的研究，但参与收缩反应的机制仍不清楚。我们研究了缝隙连接细胞和平滑肌细胞对神经介导的、三磷酸腺苷依赖的尿道平滑肌收缩的贡献。
从兔尿道平滑肌条带中进行张力记录。使用膜片钳技术从新鲜分离的平滑肌细胞和缝隙连接细胞中记录膜电位和离子电流。
刺激尿道平滑肌的壁内神经产生的收缩被广泛的 P2 受体抑制剂吡哆醛-6-偶氮苯基-2',4'-二磺酸盐和 P2X 受体激动剂 α,β-亚甲基三磷酸腺苷抑制，但不受 P2Y 受体拮抗剂 MRS2500 的影响。在保持电位为-60 mV 的电压钳下研究时，缝隙连接细胞显示出自发的瞬时内向电流，该电流的频率被三磷酸腺苷增加，但不受 α,β-亚甲基三磷酸腺苷的影响。相比之下，平滑肌细胞是静止的，但对三磷酸腺苷和 α,β-亚甲基三磷酸腺苷的反应是产生一个单一的瞬时内向电流。平滑肌细胞中由三磷酸腺苷引起的电流被 α,β-亚甲基三磷酸腺苷、吡哆醛-6-偶氮苯基-2',4'-二磺酸盐和苏拉明抑制，并被从 130 到 13 mM 的细胞外 Na+减少抑制。
刺激兔尿道平滑肌的嘌呤能神经通过激活平滑肌细胞上的 P2X 受体引起收缩。
