Histamine‐induced inward currents in cultured endothelial cells from human umbilical vein

Bregestovski, P.; Bakhramov, A.; Danilov, S.; Moldobaeva, Aigul; Takeda, Kenneth

doi:10.1111/j.1476-5381.1988.tb11663.x

Cited by 78 publications

(35 citation statements)

References 33 publications

(54 reference statements)

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“…One is activated by ATP or histamine, and the other is insensitive to these agonists and is defined as the basal non-selective cation current. The non-selective cation current induced by histamine in human umbilical vein (Bregestovski, Bakhramov, Danilov, Moldobaeva & Takeda, 1988;Nilius et al 1993) might be different from the basal non-selective cation current in the present study in terms of the sensitivity to intracellular Ca2+. (Cannell & Sage, 1989;Nilius et al 1993) or in bovine atrial EE cells ).…”

Section: Discussionmentioning

confidence: 59%

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

Manabe

Takano

Noma

1995

The Journal of Physiology

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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.

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Section: Discussionmentioning

confidence: 59%

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

Manabe

Takano

Noma

1995

The Journal of Physiology

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“…Histamine in the pipette solution was unable to elicit single-channel activity but clearly induced single-channel activity in cell-attached membrane patches if present in the bath solution. Although both extracellular and cytosolic Ca 2+ were necessary for histamine to activate the channel, Bregestovski's experiments 190 allow no unequivocal conclusion with respect to the activation mechanism. These unitary currents have also been observed in the absence of agonist, as has a higher conductance, nonselective cation channel.…”

Section: Agonist-evoked Conductance Changesmentioning

confidence: 89%

“…However, it should also be noted that, although a variety of nonselective cation channels have been described in endothelial cells ( Table Figure 3) have observed a delayed (>30 seconds) increase in inward current that developed after exposure to agonist. Bregestovski et al 190 and, more recently, Nilius and Riemann 193 have described an inward, nonselective cation current evoked by histamine in human umbilical vein endothelial cells, which showed a latency of >60 seconds and was mimicked by application of A23187 (also compare Reference 209). The unitary conductance of 20-26 pS and the reversal potential measurements suggest that the channel is nonselective, although when internal K + was replaced with Na + , only inward currents were observed.…”

Section: Agonist-evoked Conductance Changesmentioning

confidence: 99%

Intracellular calcium, currents, and stimulus-response coupling in endothelial cells.

1993

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Vascular endothelium appears to be a unique organ. It not only responds to numerous hormonal and chemical signals but also senses changes in physical parameters such as shear stress, producing mediators that modulate the responses of numerous cells, including vascular smooth muscle, platelets, and leukocytes. In many cases, the initial response of endothelial cells to these diverse signals involves elevation of cytosolic Ca 2+ and activation of Ca 2+-dependent enzymes, including nitric oxide synthase and phospholipase A 2 . Both the release of Ca 2+ from intracellular stores, most likely the endoplasmic reticulum, and the influx of Ca 2+ from the extracellular space contribute to the [Ca 2+ ]| increase. The most important trigger for Ca 2+ release is inositol 1,4,5 -trisphosphate, which is generated by the action of phospholipase C, a plasmalemmal enzyme activated in many cases by the receptor-G protein cascade. Ca 2+ influx appears to be related to the activity of receptor-G protein-enzyme complex and to the degree of fullness of the endoplasmic reticulum but does not involve voltage-gated Ca 2+ channels. The magnitude of the Ca 2+ influx depends on the electrochemical gradient, which is modulated by the membrane potential, V m . Under basal conditions, V m is dominated by a large inward rectifier K + current. Some stimuli, e.g., acetylcholine, have been shown to hyperpolarize V m , thus increasing the electrochemical gradient for Ca 2+ , which appears to be modulated by activation of Ca 2+ -dependent K + and CI" currents. However, the lack of potent and specific blockers for many of the described or postulated channels (e.g., nonselective cation channel, Ca 2+ -activated Cl~ channel) makes an estimation of their effect on endothelial cell function rather difficult. involved in the contraction of endothelial cells and the increased permeability of microvessels in response to inflammatory agents (for review, see Reference 19). Thus, a detailed knowledge of intracellular Ca 2+ homeostasis is essential for our understanding of the physiology, pathophysiology, and pharmacology of endothelial cells. The following sections review the importance of the endothelium in various disease states and the mechanisms underlying cytoplasmic Ca 2+ regulation under basal and stimulated conditions. Importance of the Endothelium in VariousDisease States Increased systemic vascular tone, which is thought to result from enhanced circulating hormones (e.g., norepinephrine, angiotensin II), is among the most common hemodynamic findings in patients with heart failure. 20 However, heightened vasoconstriction correlates poorly with the plasma levels of these substances. 20 The poor correlation could possibly be explained by the involvement of local, endothelium-dependent factors, such as an imbalance of endothelium-derived relaxing and contracting factors.21 " 23 This view is supported by numerous studies conducted in isolated vascular segments as well as in intact laboratory animals and human subjects in a variety of disease states, i...

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“…The activation of the non-selective cation channel or current (Bregestovski, Bakhramov, Danilov, Moldobaeva & Takeda, 1988;Adams et al 1989;Nilius, 1990;Nilius & Riemann, 1990) by vasoactive substances has been demonstrated in various tissues. The accompanying paper (Manabe et al 1995) studied the agonist-induced responses of the EE cells, and showed that the membrane was hyperpolarized through the activation of the Ca2+-dependent K+ channels, and concluded that the contribution of the non-selective cation channel should be minor, if any.…”

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

The Journal of Physiology

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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.

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Histamine‐induced inward currents in cultured endothelial cells from human umbilical vein

Cited by 78 publications

References 33 publications

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

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

Intracellular calcium, currents, and stimulus-response coupling in endothelial cells.

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

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