The autonomic and sensory innervation of the smooth muscle of the prostategland: a review of pharmacological and histological studies

Citation
Jn. Pennefather et al., The autonomic and sensory innervation of the smooth muscle of the prostategland: a review of pharmacological and histological studies, J AUT PHARM, 20(4), 2000, pp. 193-206
Citations number
159
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF AUTONOMIC PHARMACOLOGY
ISSN journal
01441795 → ACNP
Volume
20
Issue
4
Year of publication
2000
Pages
193 - 206
Database
ISI
SICI code
0144-1795(200008)20:4<193:TAASIO>2.0.ZU;2-R
Abstract
1 We review literature demonstrating (a) the presence and (b) the actions o f substances that mediate or modify neuroeffector transmission to the smoot h muscle of the prostrate stroma of a number of species including man. 2 In all species studied prostatic stroma, but not secretory acini, receive s rich noradrenergic innervation. Stimulation of these nerves causes contra ctions of prostate smooth muscle that are inhibited by guanethidine and by alpha (1)-adrenoceptor antagonists that probably act at the alpha (1L)-adre noceptor. Such actions underlie the clinical use of alpha (1)-adrenoceptor antagonists in benign prostatic hyperplasia (BPH). 3 Acetylcholinesterase-positive nerves innervate prostatic stroma as well a s epithelium. Atropine reduces nerve-mediated contractions of stromal muscl e in the rat, guinea-pig and rabbit. M-1, M-2 and M-3 muscarinic receptors have been implicated in eliciting or facilitating contraction in the prosta te from guinea-pig, dog and rat, respectively. 4 Adenine nucleotides and nucleosides, nitric oxide (NO), opioids, neuropep tide Y (NPY) and vasoactive intestinal peptide (VIP), may act as co-transmi tters or modulators in autonomic effector nerves supplying prostate stroma. Adenosine inhibits neurotransmission to the rat prostate, and NO is inhibi tory in prostate from human, rat, rabbit, pig and dog. The activity of pept ides present in the relatively sparse sensory innervation of the prostate e xhibits species variation, but, when effective, calcitonin gene-related pep tide is inhibitory while tachykinins are stimulant. The roles of NPY and VI P in modulating stromal contractility remain unclear. 5 Taken together the current literature indicates that, in addition to nora drenaline, other neurotransmitters and neuromodulators may regulate the ton e of prostatic smooth muscle. Whether drugs that mimic or modify their acti ons might be useful in providing symptomatic relief of the urinary symptoms associated with BPH remains to be established.