Hannover Medical School-Division of Surgery, Department of Urology and Urological Oncology, Hannover, Germany.
Hannover Medical School-Division of Surgery, Department of Urology and Urological Oncology, Hannover, Germany.
J Sex Med. 2010 Jun;7(6):2104-2111. doi: 10.1111/j.1743-6109.2010.01808.x. Epub 2010 May 11.
The cyclic adenosine monophosphate-dependent protein kinase (cAK) is considered a key protein in the control of smooth muscle tone in the cardiovascular system. There is evidence that erectile dysfunction might be linked to systemic vascular disorders and arterial insufficiency, subsequently resulting in structural changes in the penile tissue. The expression and significance of cAK in human cavernous arteries (HCA) have not been evaluated.
To evaluate the expression of cAK isoforms in HCA and examine the role of cAK in the cyclic adenosine monophosphate (cAMP)- and cyclic guanosine monophosphate (cGMP)-mediated control of penile vascular smooth muscle.
The expression and distribution of phosphodiesterase type 4 (PDE4) and cAK isoforms in sections of HCA were investigated by means of immunohistochemistry and Western blot analysis. The effects of the cAK inhibitor Rp-8-CPT-cAMPS on the relaxation of isolated preparations of HCA (diameter > 100 µm) induced by rolipram, sildenafil, tadalafil, and vardenafil were studied using the organ bath technique.
Investigate the expression of cAK in relation to α-actin and PDE4 in HCA and evaluate the effects of an inhibition of cAK on the relaxation induced by inhibitors of PDE4 and PDE5 of isolated penile arteries.
Immunosignals specific for cAKIα, IIα, and IIβ were observed within the wall of HCA. Double stainings revealed colocalization of cAK with α-actin and PDE4. The expression of cAK isoforms was confirmed by Western blot analysis. The reversion of tension induced by inhibitors of PDE4 and PDE5 of isolated penile vascular tissue were attenuated significantly by Rp-8-CPT-cAMPS.
Our results demonstrate the expression of cAK isoforms in the smooth musculature of HCA and its colocalization with PDE4. A significant role for cAK in the regulation mediated by cAMP and cGMP of vascular smooth muscle tone in HCA can also be assumed.
环磷酸腺苷依赖性蛋白激酶（cAK）被认为是控制心血管系统平滑肌张力的关键蛋白。有证据表明，勃起功能障碍可能与全身血管疾病和动脉功能不全有关，随后导致阴茎组织的结构变化。cAK 在人海绵体动脉（HCA）中的表达和意义尚未得到评估。
评估 cAK 同工型在 HCA 中的表达，并研究 cAK 在环磷酸腺苷（cAMP）和环鸟苷酸（cGMP）介导的阴茎血管平滑肌控制中的作用。
通过免疫组织化学和 Western blot 分析研究了 HCA 中磷酸二酯酶 4（PDE4）和 cAK 同工型的表达和分布。使用器官浴技术研究了 cAK 抑制剂 Rp-8-CPT-cAMPS 对罗利普兰、西地那非、他达拉非和伐地那非诱导的 HCA（直径>100μm）分离标本松弛的影响。
研究 cAK 与 HCA 中的α-肌动蛋白和 PDE4 的关系，并评估 cAK 抑制对 PDE4 和 PDE5 抑制剂诱导的分离阴茎动脉松弛的影响。
在 HCA 壁内观察到特异性的 cAKIα、IIα 和 IIβ 免疫信号。双重染色显示 cAK 与α-肌动蛋白和 PDE4 共定位。Western blot 分析证实了 cAK 同工型的表达。Rp-8-CPT-cAMPS 显著减弱了 PDE4 和 PDE5 抑制剂诱导的分离阴茎血管组织张力的恢复。
我们的结果表明 cAK 同工型在 HCA 的平滑肌中表达，并与 PDE4 共定位。cAK 在 cAMP 和 cGMP 介导的 HCA 血管平滑肌张力调节中也可能发挥重要作用。
