A target K+ channel for the LP-805-induced hyperpolarization in smooth muscle cells of the rabbit portal vein

1993 ◽  
Vol 347 (3) ◽  
pp. 329-335 ◽  
Author(s):  
Masahiro Kamouchi ◽  
Shunichi Kajioka ◽  
Takeshi Sakai ◽  
Kenji Kitamura ◽  
Hirosi Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
K Channel ◽  
Rabbit Portal Vein

scholarly journals LP-805 opens a glibenclamide-sensitive K channel in dispersed smooth muscle cells of the rabbit portal vein

1992 ◽  
Vol 58 ◽  
pp. 283
Author(s):  
Masahiro Kamouchi ◽  
Shunichi Kajioka ◽  
Kenji Kitamura ◽  
Hirosi Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
K Channel ◽  
Rabbit Portal Vein

β-Adrenoceptor activation and PKA regulate delayed rectifier K+ channels of vascular smooth muscle cells

1998 ◽  
Vol 275 (2) ◽  
pp. H448-H459 ◽  
Author(s):  
E. Alejandro Aiello ◽  
A. Todd Malcolm ◽  
Michael P. Walsh ◽  
William C. Cole
Keyword(s):  
Signal Transduction ◽  
Smooth Muscle ◽  
Portal Vein ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Catalytic Subunit ◽  
Delayed Rectifier ◽  
Rabbit Portal Vein

Macroscopic 4-aminopyridine (4-AP)-sensitive, delayed rectifier K+ current of vascular smooth muscle cells is increased during β-adrenoceptor activation with isoproterenol via a signal transduction pathway involving adenylyl cyclase and cAMP-dependent protein kinase (PKA) (Aiello, E. A., M. P. Walsh, and W. C. Cole. Am. J. Physiol. 268 ( Heart Circ. Physiol. 37): H926–H934, 1995.). In this study, we identified the single delayed rectifier K+(KDR) channel(s) of rabbit portal vein myocytes affected by treatment with isoproterenol or the catalytic subunit of PKA. 4-AP-sensitive KDR channels of 15.3 ± 0.6 pS ( n = 5) and 14.8 ± 0.6 pS ( n = 5) conductance, respectively, were observed in inside-out (I-O) and cell-attached (C-A) membrane patches in symmetrical KCl recording conditions. The kinetics of activation (time constant of 10.7 ± 3.02 ms) and inactivation (fast and slow time constants of 0.3 and 2.5 s, respectively) of ensemble currents produced by these channels mimicked those reported for inactivating, 4-AP-sensitive whole cell KDR current of vascular myocytes. Under control conditions, the open probability ( NP o) of KDR channels of C-A membrane patches at −40 mV was 0.014 ± 0.005 ( n = 8). Treatment with 1 μM isoproterenol caused a significant, approximately threefold increase in NP o to 0.041 ± 0.02 ( P < 0.05). KDR channels of I-O patches exhibited rundown after ∼5 min, which was not affected by ATP (5 mM) in the bath solution. Treatment with the purified catalytic subunit of PKA (50 nM; 5 mM ATP) restored KDRchannel activity and caused NP o to increase from 0.011 ± 0.003 to 0.138 ± 0.03 ( P < 0.05; n = 11). These data indicate that small-conductance, 15-pS KDRchannels are responsible for inactivating the macroscopic delayed rectifier K+ current of rabbit portal vein myocytes and that the activity of these channels is enhanced by a signal transduction mechanism involving β-adrenoceptors and phosphorylation by PKA at a membrane potential consistent with that observed in the myocytes in situ.

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