POSSIBLE ROLE OF DISTURBED NA-DEFERENS CONTRACTILE HYPERREACTIVITY AFTER IMMUNOLOGICAL SENSITIZATION( HOMEOSTASIS IN MOUSE VAS)

Citation
O. Souilem et al., POSSIBLE ROLE OF DISTURBED NA-DEFERENS CONTRACTILE HYPERREACTIVITY AFTER IMMUNOLOGICAL SENSITIZATION( HOMEOSTASIS IN MOUSE VAS), Naunyn-Schmiedeberg's archives of pharmacology, 358(4), 1998, pp. 474-482
Citations number
41
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00281298
Volume
358
Issue
4
Year of publication
1998
Pages
474 - 482
Database
ISI
SICI code
0028-1298(1998)358:4<474:PRODNC>2.0.ZU;2-C
Abstract
In the present study we have investigated the involvement of sensitize d mice immunoglobulins and some electrophysiological alterations that participate to the antigenic sensitization-induced hyperreactivity of isolated mouse vas deferens. Active sensitization was performed by sub cutaneous injection of egg albumen. Contractile responses to noradrena line were isometrically recorded in the isolated vas deferens. Low ext ernal Na+-induced contractions and rapid cooling contractures were eva luated. Resting membrane potential (Er) and intracellular Na activity were measured in control and actively sensitized vas deferens by using conventional KCl-filled and Na+-sensitive microelectrodes respectivel y. Active sensitization-induced hyperreactivity to noradrenaline was r eproduced by in vitro passive sensitization of control MS deferens wit h sensitized mice immunoglobulins. The inhibition of the nitric oxide synthesis by N-nitro-L-arginine methyl ester (L-NAME) did not change c ontrol vas deferens reactivity in vitro to noradrenaline and acetylcho line. Rapid cooling contractures, performed after lowering external Na + concentration, were not altered by active sensitization. However, se nsitization increased significantly the strength of the low external N a+-induced contractions. In control vas deferens Er was a mean of -49. 2+/-0.3 mV (mean +/-SEM). Sensitization resulted in reduction of Er by 14 mV. In sensitized preparations, relative insensitivity of Er to ou abain, external K+ removal and cooling were observed. The intracellula r Na+ activity was increased by about 40% in sensitized vas deferens. It is concluded that sensitization-induced hyperreactivity is mediated by immunoglobulins and produced smooth muscle cells depolarisation. T he low Er of sensitized muscle may be partly the result of an increase in membrane permeability to Na+ which could interface with intracellu lar Ca2+ homeostasis.