Literature DB >> 9138243

Heme oxygenase and NO-synthase in the human prostate--relation to adrenergic, cholinergic and peptide-containing nerves.

P Hedlund1, P Ekström, B Larsson, P Alm, K E Andersson.   

Abstract

In the human prostate, the distribution of heme oxygenase (HO-1 and HO-2)-, nitric oxide synthase (NOS)-, and tyrosine hydroxylase (TH)-immunoreactive (IR), acetylcholine-esterase (AChE)-positive, and some peptidergic nerve structures was investigated. Cell bodies and nerve fibers within coarse nerve trunks expressed HO-1-, HO-2-, NOS-, TH-, and vasoactive intestinal polypeptide (VIP)-immunoreactivities, and were AChE-positive, but, as revealed by confocal microscopy. HO- and NOS-immunoreactivities were found in separate nerves. Along strains of smooth muscle, intraglandular septa, and around acini, HO-1-, NOS-, and VIP-IR nerves, and AChE-positive fibers were observed. Double immunostaining showed that NOS- and VIP-immunoreactivities were generally co-localized in varicose nerve terminals. Some TH-IR terminals had profiles that were similar, but not identical, to those of NOS-, HO-1-, or VIP-IR terminals. NPY-IR nerves were similarly distributed as VIP- and NOS-IR fibers, and were found in rich amounts. Calcitonin gene-related peptide (CGRP)-IR nerves were few compared to other nerve populations studies. NOS- and CGRP-IR terminals had similar profiles, but the immunoreactivities were not co-localized. Nitric oxide and electrical stimulation of nerves relaxed noradrenaline-contracted preparations of prostatic stroma. Inhibition of synthesis of nitric oxide abolished the electrically induced relaxations. VIP had small relaxant effects, whereas carbon monoxide was without effect on noradrenaline-contracted strips. The innervation pattern and the functional effects suggest that the L-arginine/nitric oxide pathway may have a role in the control of human prostatic smooth muscle activity and/or in secretory neurotransmission. A physiological role of carbon monoxide in the prostate remains to be established.

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Year:  1997        PMID: 9138243     DOI: 10.1016/s0165-1838(96)00139-7

Source DB:  PubMed          Journal:  J Auton Nerv Syst        ISSN: 0165-1838


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