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
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.