Dept. of Biomedical Engineering, Duke University, Box 90281, Durham, NC 27708-0281, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Feb;300(2):R398-407. doi: 10.1152/ajpregu.00154.2010. Epub 2010 Nov 10.
Activation of pudendal afferents can evoke bladder contraction or relaxation dependent on the frequency of stimulation, but the mechanisms of reflex bladder excitation evoked by pudendal afferent stimulation are unknown. The objective of this study was to determine the contributions of sympathetic and parasympathetic mechanisms to bladder contractions evoked by stimulation of the dorsal nerve of the penis (DNP) in α-chloralose anesthetized adult male cats. Bladder contractions were evoked by DNP stimulation only above a bladder volume threshold equal to 73 ± 12% of the distension-evoked reflex contraction volume threshold. Bilateral hypogastric nerve transection (to eliminate sympathetic innervation of the bladder) or administration of propranolol (a β-adrenergic antagonist) decreased the stimulation-evoked and distension-evoked volume thresholds by -25% to -39%. Neither hypogastric nerve transection nor propranolol affected contraction magnitude, and robust bladder contractions were still evoked by stimulation at volume thresholds below the distension-evoked volume threshold. As well, inhibition of distention-evoked reflex bladder contractions by 10 Hz stimulation of the DNP was preserved following bilateral hypogastric nerve transection. Administration of phentolamine (an α-adrenergic antagonist) increased stimulation-evoked and distension-evoked volume thresholds by 18%, but again, robust contractions were still evoked by stimulation at volumes below the distension-evoked threshold. These results indicate that sympathetic mechanisms contribute to establishing the volume dependence of reflex contractions but are not critical to the excitatory pudendal to bladder reflex. A strong correlation between the magnitude of stimulation-evoked bladder contractions and bladder volume supports that convergence of pelvic afferents and pudendal afferents is responsible for bladder excitation evoked by pudendal afferents. Further, abolition of stimulation-evoked bladder contractions following administration of hexamethonium bromide confirmed that contractions were generated by pelvic efferent activation via the pelvic ganglion. These findings indicate that pudendal afferent stimulation evokes bladder contractions through convergence with pelvic afferents to increase pelvic efferent activity.
阴部传入纤维的激活可以根据刺激频率引起膀胱收缩或松弛，但阴部传入刺激引起反射性膀胱兴奋的机制尚不清楚。本研究的目的是确定在氯醛糖麻醉的成年雄性猫中，刺激阴茎背神经（DNP）时，交感和副交感机制对膀胱收缩的贡献。只有在膀胱容积阈值等于充盈诱发反射收缩容积阈值的 73±12%以上时，DNP 刺激才能诱发膀胱收缩。双侧下腹神经切断（消除膀胱的交感神经支配）或给予普萘洛尔（β-肾上腺素能拮抗剂）可使刺激诱发和充盈诱发的容积阈值降低 25%至 39%。下腹神经切断或普萘洛尔均不影响收缩幅度，并且在低于充盈诱发容积阈值的容积阈值下仍可通过刺激诱发强烈的膀胱收缩。此外，双侧下腹神经切断后，DNP 10Hz 刺激抑制充盈诱发的反射性膀胱收缩仍然存在。给予酚妥拉明（α-肾上腺素能拮抗剂）可使刺激诱发和充盈诱发的容积阈值增加 18%，但在低于充盈诱发阈值的容积下仍可通过刺激诱发强烈的收缩。这些结果表明，交感机制有助于建立反射收缩的容积依赖性，但对于兴奋性阴部至膀胱反射并非至关重要。刺激诱发的膀胱收缩幅度与膀胱容积之间存在很强的相关性，支持盆部传入纤维和阴部传入纤维的会聚是阴部传入纤维引起膀胱兴奋的原因。进一步，给予六烃季铵溴化物后刺激诱发的膀胱收缩消失，证实了收缩是通过盆神经节激活盆部传出纤维产生的。这些发现表明，阴部传入刺激通过与盆部传入纤维的会聚引起膀胱收缩，从而增加盆部传出纤维的活动。
