B. Vanheel et J. Van De Voorde, Barium decreases endothelium-dependent smooth muscle responses to transient but not to more prolonged acetylcholine applications, PFLUG ARCH, 439(1-2), 1999, pp. 123-129
The influence of inhibiting the inward rectifier and Na/K pump on endotheli
um-dependent hyperpolarizations in smooth muscle cells of the mesenteric ar
tery was investigated. Membrane potential was measured with microelectrodes
, and the influence of low concentrations of Ba2+ (30 mu M) and of high con
centrations of ouabain (0.5 mM) on smooth muscle hyperpolarization elicited
by prolonged or by transient exposure to acetylcholine (ACh, 3x10(-7) M) w
as assessed in the continuous presence of NC-nitro-L-arginine (100 mu M) an
d indomethacin (50 mu M). Pre-exposure to Ba2+ did not inhibit the magnitud
e of smooth muscle cell hyperpolarization induced by ACh superfusion, but s
ignificantly slowed its onset and time course. The membrane potential respo
nse to transient ACh applications, however, was impaired. After combined Ba
2+ and ouabain pre-exposure, peak hyperpolarizations to ACh superfusion wer
e somewhat decreased but not abolished. In addition, 4-5 mM increases of th
e extracellular K+ concentration consistently depolarized:smooth muscle cel
ls. These findings argue against the idea that smooth muscle inward rectifi
er K+ channels and Na/K pumping play a role in the ACh-induced endothelium-
dependent hyperpolarization of this preparation. Moreover, the slowing of s
mooth muscle membrane hyperpolarization by Ba2+ is discussed in terms of th
e influence of this ion on the release of hyperpolarizing factor.