Permeability and Mg2+ blockade of histamine‐operated cation channel in endothelial cells of rat intrapulmonary artery.

1. Endocardial endothelial (EE) cells, isolated by the enzymatic treatment of guinea-pig heart, were used for whole-cell voltage clamp experiments. 2. The inward rectifier K+ current was observed in about half of the experiments. The contribution of Ca2+-dependent K+ current to the resting membrane conductance was also suggested. 3. After the K+ conductances were suppressed, removal of external Na+ revealed an inward cation current (12 pA pF-, at -45 mV), whose slope conductance was a saturable function of external Na+ concentration. When Na+ was totally replaced by various monovalent cations, the order of the membrane conductances was K+ > Rb+ > Cs+ > Na+ > Li+. 4. This basal non-selective cation current was blocked by either Gd3+ or La3+, and showed slight outward rectification. 5. Addition of 20 mm Ca2+ or Ba2+, but not Mg2+ or Mn2+, to the Na+-free solution, induced an inward current, indicating that this current possesses a significant Ca2+ permeability. 6. In -15% of the experiments, ATP and histamine induced another type of non-selective cation current, which showed different ion selectivity (Na+> K+, Cs+) and rectification (inward). 7. The basal non-selective cation current is responsible for both the low resting potential and the leak Ca2P influx of EE cells.

Section: Resultsmentioning

confidence: 99%

Non‐selective cation current of guinea‐pig endocardial endothelial cells.

Manabe

Takano

Noma

1995

“…Corresponding types of ion channels have been described in vascular endothelial cells as follows. Non-selective cation channels recorded in the luminal membrane of different intact endothelial cells share several common properties (Yamamoto et al 1992;Ito et al 1993; this study). The channels showed significant open probability at the resting membrane potential and were activated on strong depolarization.…”

Section: Discussionmentioning

confidence: 99%

Classification of ion channels in the luminal and abluminal membranes of guinea‐pig endocardial endothelial cells.

Manabe¹,

Ito²,

Matsuda³

et al. 1995

1. The ion channels on both the luminal and abluminal membranes of endocardial endothelial (EE) cells were separately recorded using the patch clamp technique in the guinea-pig heart.2. The major population consisted of two types of non-selective cation channels, which showed open probabilities of 0-21 and 0 33 at the resting potential, and conductances of 36 and 11 pS, respectively. 3. The next major class was Cl-channels with an ohmic conductance of 409 pS. The channel was quiescent in the cell-attached mode but was activated by strong depolarization after excising the patch membrane.4. The channels activated by intracellular Ca2+ were mainly K+ channels showing a 34 pS slope conductance and, less frequently, Ca2+-dependent K+ channels having a large conductance (210 pS). The inward rectifier K+ channel (32 pS) was also observed. 5. The non-selective cation channels were recorded on the luminal membrane, but scarcely on the abluminal membrane, suggesting an active transport of K+ and Na+ across the endocardium. 6. The resting membrane conductance of the EE cells may be provided mostly by nonselective cation channels and 34 pS Ca2+-dependent K+ channels.

“…They are thought to take part in important physiological roles such as excitationsecretion coupling, or neuron and cardiac muscle cell excitability (Partridge & Swandulla, 1988;Thorn & Petersen, 1993). In endothelial cells, various non-selective cation channels of moderate conductance have been described, but these are generally insensitive to Ca2+ (Yamamoto et al 1992;Adams, 1994). Nilius et at.…”

mentioning

confidence: 99%

“…In these cells, the bradykinin-induced rise in cytosolic Ca2+ is reduced by 70-80% in the absence of extracellular Cam+ and markedly shortened (see also Buclhan & Martin, 1991;Sturek et al 1991 Some endothelial cation channels are more selective for Ca2+ than the Ca2P-dependent cation channel we described for the coronary artery. For example, the stretch-activated channels can be 12 times more permeable to Ca2+ than to Na+ or K+, the histamine-operated cation channel shows a 16 times higher permeabilityr to Ca2+ than to K+ and Na+ in the intrapulmnonary artery, and the CRAC channel, activated by histamine or bradykinin, should also be highly permeable to Ca2+ (Yamamoto et al 1992;Nilius et al 1993;Adams, 1994). However, Ca2 -dependent cation channels seem to be present with a high density in coronary artery endothelial cells, which argues for a major physiological role in endothelial cell activation.…”

mentioning

confidence: 99%

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

Baron¹,

Frieden²,

Chabaud³

et al. 1996

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