Sparwasser C, Drescher P, Eckert R, Madsen P O
Veterans Administration Hospital, Madison, WI, USA.
Urol Res. 1995;22(6):393-8. doi: 10.1007/BF00296883.
Norepinephrine release from adrenergic nerve terminals leads to a rise in intracellular Ca2+, which promotes penile smooth muscle contraction and detumescence. Ca2+ sources are the extracellular space and sarcoplasmic Ca2+ stores. To elucidate the role of intracellular stores strips from rabbit erectile tissue were investigated in an organ bath study. Contractions were elicited by phenylephrine (PE) and electrical stimulation. Incubation in Ca(2+)-free solution as well as exposure to nifedipine did not abolish electrical or PE-induced contraction. Ryanodine (10(-5) mol/l), a functional blocker of sarcoplasmic Ca2+ channels, significantly reduced PE response. In the presence of caffeine (10(-3) mol/l) the effect was significantly enhanced. Addition of nifedipine nearly abolished the contraction. These results provide evidence for intracellular Ca2+ pools in cavernosal tissue and indicate that the alpha 1-adrenoceptor-induced contraction requires the opening of voltage-gated Ca2+ channels and the release of Ca2+ from intracellular stores.
去甲肾上腺素能神经末梢释放的去甲肾上腺素会导致细胞内Ca2+浓度升高,从而促进阴茎平滑肌收缩和消肿。Ca2+的来源是细胞外空间和肌浆Ca2+储存库。为了阐明细胞内储存库的作用,在器官浴研究中对来自兔勃起组织的条带进行了研究。用去氧肾上腺素(PE)和电刺激引发收缩。在无Ca(2+)溶液中孵育以及暴露于硝苯地平并不能消除电刺激或PE诱导的收缩。Ryanodine(10(-5) mol/l),一种肌浆Ca2+通道的功能性阻滞剂,显著降低了PE反应。在咖啡因(10(-3) mol/l)存在的情况下,这种作用显著增强。添加硝苯地平几乎消除了收缩。这些结果为海绵体组织中的细胞内Ca2+池提供了证据,并表明α1-肾上腺素能受体诱导的收缩需要电压门控Ca2+通道的开放以及细胞内储存库中Ca2+的释放。