Ca(2+)‐dependent non‐selective cation and potassium channels activated by bradykinin in pig coronary artery endothelial cells.

Abstract

1. Using the cell-attached and inside-out modes of the patch-clamp technique, we studied the Ca2+-dependent ionic channels activated by bradykinin in cultured pig coronary artery endothelial cells to further understand electrophysiological events underlying cellular activation.2. In the cell-attached mode, bradykinin (94 nM) activated two types of Ca2P-dependent channels: a high conductance K+ channel (285 pS in high symmetrical K+), whose open state probability was increased by depolarization, and a lower conductance inwardly rectifying non-selective cation channel (44 pS in high symmetrical K+). with nearly the same permeability (P) as monovalent cations (PK: PNa: Pca= 1: 1: 07). 6. The cation channel appeared to be more sensitive to Ca2+ than the K+ channel, with a halfmaximal open probability induced by 0 7 gm Ca2P on the intracellular side of the membrane. 7. In contrast to the K+ channel, the cation channel mean open time was clearly increased by bradykinin. This effect was delayed compared with the increase in the channel open state probability and was rapidly lost in the inside-out configuration. Caffeine also activated the cation channel but more transiently than bradykinin and without any effect on the open duration.8. In the absence of extracellular Ca2+, the bradykinin-induced increase in cytosolic free Ca2+ was shortened temporally by 52% and reduced in amplitude by 88%, whereas the bradykinin-induced hyperpolarization was not significantly reduced in amplitude but was shortened by 70%, thus illustrating the major role of Ca2P influx in endothelial cell activation by bradykinin. 9. We conclude that bradykinin activates two types of

Cilostazol Suppresses Superoxide Production and Expression of Adhesion Molecules in Human Endothelial Cells via Mediation of cAMP-Dependent Protein Kinase-Mediated Maxi-K Channel Activation

“…Most recently, cilostazol was shown to increase the outward K ϩ currents in SK-N-SH cells (human brain neuroblastoma cells) (Hong et al, 2003) by the opening of the maxi-K ϩ channels. On the other hand, the presence of BKCa channels has been shown in many types of endothelial cells (Rusko et al, 1992;Baron et al, 1996;Nilius et al, 1997), as well as in the EA.hy926 cell line (Haburcak et al, 1997). The maxi-K channel mRNA expression of the ␣-subunit, but not the ␤-subunit, was detected in the endothelium (Papassotiriou et al, 2000).…”

An evaluation of potassium ions as endothelium‐derived hyperpolarizing factor in porcine coronary arteries

“…This hyperpolarization reaches a maximum close to the equilibrium potential of potassium ion when E K is changed by manipulating extracellular potassium concentration (Brunet & Be ny, 1989). In addition, whole cell and single channel patch clamp experiments showed that the kinins gate calcium-dependent potassium channels and that the transient current elicited by the peptides is a potassium current (Baron et al, 1996;1997). Therefore the stimulation of the endothelial cells by the kinins leads to the opening of potassium channels and consequently to a release of potassium ions.…”

Interaction of d-Tubocurarine with Potassium Channels: Molecular Modeling and Ligand Binding

“…These rough estimates do not take into consideration the flexibility of d-tubocurarine and the channels. d-Tubocurarine is known to block large conductance Ca 2ϩ -and voltage-activated K ϩ channels (BKs) in micromolar concentrations from the cytoplasmic side (Egan et al, 1993;Baron et al, 1996). However, no data are available on d-tubocurarine binding to Kv channels.…”