ABSTRACT
The acetylcholine-induced hyperpolar iza t ion may depend on the act ivat ion o f K + - channels, since the ampli tude o f the potential inversely relates to the concentrat ion o f potassium ions i n the solut ion (Chen et al, 1988; C h e n and Suzuk i , 1989). The inh ib i t ion o f this hyperpolar iza t ion by charybdotox in and apamin, but not by glibenclamide, B a 2 + or 4-aminopyridine, suggests that the ma in K + - c h a n n e l s activated are o f Ca 2 + - s ens i t i ve type ( M u r p h y and Brayden, 1995; M a r c h e n c o and Sage, 1996; Hash i t an i and Suzuk i , 1997; N i s h i y a m a et al, 1998). Myo-endo the l i a l gap junct ions exist (Chaytor et al, 1998), and functional communica t ion between endothelial and smooth muscle cells has been confirmed using dyes transferable through gap junct ions (Li t t le et al, 1995). M e m b r a n e potential changes occurr ing i n endothelial cells can be propagated to smooth muscle cells through gap junct ions (Bény and Pacicca, 1994), and the opposite is also the case ( Y a m a m o t o et al, 1999). These observations suggest that the dis t r ibut ion o f K + - c h a n n e l s activated by acetylcholine is difficult to determine in experiments using convent ional microelectrode techniques alone.
