| Literature DB >> 3968758 |
A Mattiasson, K E Andersson, C Sjögren.
Abstract
Isolated urethral muscle from rabbit and man was subjected to electrical field stimulation and the components of the resulting contraction were analyzed. Contraction usually consisted of 2 main components. One was rapidly developing, non-adrenergic and atropine-resistant. The other developed more slowly and was sensitive to alpha-adrenoceptor blockade and to chemical sympathectomy with 6-hydroxydopamine. By lowering the temperature from 37C to 20C, these contraction components could be separated from each other. Both could be blocked by tetrodotoxin but the effects of this drug were not consistent in human tissue. Characteristic for the initial contraction component was its dependence on the tension of the preparation; it increased with increasing tension. The adrenergic part of the contraction could be effectively blocked by phentolamine and prazosin, whereas rauwolscine was less effective. Atropine and scopolamine also inhibited the adrenergic part of the contraction, whereas acetylcholine caused a transient increase. The non-adrenergic contraction component was less sensitive to deprivation of extracellular Ca2+ than the adrenergic; almost 40 per cent remained after exposure to Ca2+ free solution for 40 min., whereas the adrenergic component disappeared after 20 min. exposure. Light and electron microscopic investigation revealed 3 distinct layers of the rabbit urethral wall, 1 outer consisting of smooth and striated muscle, 1 middle consisting of smooth muscle only, and a submucosal layer where vessels and smooth muscle cells were found. Removal of the longitudinal muscle layer did not change the responses to electrical stimulation. The results suggest that the electrically induced adrenergic activation of urethral muscle of both rabbit and man was mediated mainly via alpha-adrenoceptors and that this muscle is innervated not only by sympathetic, adrenergic nerves but also by a type of nerve able to release a non-cholinergic, contraction-mediating transmitter.Entities:
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Year: 1985 PMID: 3968758 DOI: 10.1016/s0022-5347(17)48927-0
Source DB: PubMed Journal: J Urol ISSN: 0022-5347 Impact factor: 7.450