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. 2014 Apr-Jun;30(2):181–188. doi: 10.4103/0970-1591.126903

Figure 2.

Figure 2

Mechanisms of prostate smooth muscle contraction and assumed connections to the regulation of prostate growth. In contrast to earlier concepts, α1-adrenoceptors in the prostate are no longer regarded as isolated receptors mediating exclusively contraction. In fact, α1-adrenoceptors in the prostate are part of a signaling network, where different receptors and non-adrenergic mediators cooperatively regulate prostate smooth muscle tone and growth, leading to benign prostate obstruction. Prostate α1-adrenoceptors lead to contraction by activation of the IP3/Ca2+/calmodulin pathway, of DAG/protein kinase C, of the RhoA/Rho kinase pathway, and by a JNK-dependent mechanism. At least the Ca2+- and Rho kinase-dependent mechanisms are shared by TXA2 receptors, which cause prostate smooth muscle contraction in parallel to α1-adrenoceptors. In addition, α1-adrenoceptors share intracellular effectors with hormone receptors and growth factors (e. g. fibroblast growth factor): Stimulation of prostate α1-adrenoceptors leads to activation of ERK1/2, Akt and transcription factors, which are well known to mediate growth and differentiation