Passive electrical properties and electrogenic sodium transport of cultured guinea‐pig coronary endothelial cells.

Daut, Jürgen; Mehrke, G; Nees, S.; Newman, Walter H.

doi:10.1113/jphysiol.1988.sp017202

Cited by 71 publications

(68 citation statements)

References 28 publications

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“…However, the low resting potential suggests the presence of an analogous nonselective cation current system in vascular endothelial cells. In fact, the input resistance (about 5 GQI) obtained in the present study is comparable to those described in vascular endothelial cells (Johns et al 1987;Daut et al 1988). Furthermore, the existence of a leak current, which is blocked by Ni2+, has been demonstrated in human umbilical vein with a reversal potential of around 0 mV (Nilius et al 1993).…”

Section: Discussionsupporting

confidence: 70%

“…Voltage clamp experiments Single cells or clusters of two to three cells were used for whole-cell voltage clamp experiments, and perfused with the control Tyrode solution for 5-15 min before starting the experiments. The use of clusters of cells was justified as demonstrated in previous studies (Daut, Mehrke, Nees & Newman, 1988;Mendelowitz, Bacal & Kunze, 1992;Manabe et al 1995a) and in Fig. 1 of the present study.…”

Section: Solutionsmentioning

confidence: 68%

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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: Discussionsupporting

confidence: 70%

Section: Solutionsmentioning

confidence: 68%

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

Manabe

Takano

Noma

1995

The Journal of Physiology

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“…16 In addition, direct electrotonic interaction between endothelial and vascular smooth muscle cells (VSMCs) has also been proposed. 17 - 18 The intracellular signal that links systemic or local external stimuli to the synthesis and release of EDRF and prostaglandins appears to be the level of free cytosolic calcium, [Ca 2+ ]j. Furthermore, [Ca 2+ ]| also seems to be involved in the contraction of endothelial cells and the increased permeability of microvessels in response to inflammatory agents (for review, see Reference 19).…”

Section: Tutorial In Molecular and Cellular Biologymentioning

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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“…4). Further details about the apparatus and about the identification of coronary endothelial cells are given in Daut, Mehrke, Nees & Newman (1988) and in Mehrke & Daut (1990 (10-30 cmH2O) and the patch was ruptured by repetitive negative current pulses. The resting potential of monolayers AOR TIC AND CORONARY ENDOTHELIUM of BAECs ranged between -10 and -98 mV (see below).…”

Section: Introductionmentioning

confidence: 99%

Effects of vasoactive agonists on the membrane potential of cultured bovine aortic and guinea‐pig coronary endothelium.

Mehrke¹,

Pohl²,

Daut³

1991

The Journal of Physiology

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SUMMARY1. The effects of bradykinin, ATP, adenosine, histamine and thrombin on the membrane potential of confluent monolayers of cultured bovine aortic endothelial cells (BAECs) and guinea-pig coronary endothelial cells (GCECs) were studied at 37°C using the whole-cell mode of the patch-clamp technique.2. The amplitude histogram of the resting potentials of BAEC monolayers showed a bimodal distribution with one peak around -25 mV and another peak around -85 mV. Transitions from one potential level to the other were observed. The bistable membrane potential can be explained by an N-shaped current-voltage relation of the endothelial cell membrane.3. When BAECs with a low resting potential (-10 to -30 mV) were superfused with maximally effective concentrations of ATP (2-10 ,tM) an initial hyperpolarization of -80 to -90 mV was observed which decayed to a plateau of about -60 mV within min. When ATP was removed after 2-3 min the membrane potential returned to control level within 1 min. This was followed by a second hyperpolarization of 10-20 mV, which decayed within 15 min.4. In the absence of extracellular calcium, ATP produced only a brief transient hyperpolarization in aortic endothelium. The plateau and the secondary hyperpolarization were abolished. These findings are consistent with the idea that the changes in membrane potential reflect changes in intracellular free Ca2+ and that the initial peak is due to release of Ca2+ from intracellular stores, whereas the plateau and the secondary hyperpolarization depend on transmembrane Ca2+ influx.5. Bradykinin evoked potential changes similar to ATP in BAECs, except that the secondary hyperpolarization during wash-out was absent. When the membrane potential was more negative than -80 mV, ATP and bradykinin induced only a small initial hyperpolarization followed by a depolarization of up to 20 mV.6. In aortic endothelium, ADP (10 /LM) evoked a much smaller response than ATP. G. MEHRKE, U. POHL AND J. DA UT Adenosine (10 fM), thrombin (2 units/ml), acetylcholine (10 JM) and histamine (10 gM) had only a very small effect on the membrane potential, if any.7. The amplitude histogram of the membrane potential of GCECs showed only one peak around -35 mV. In coronary endothelium, application of bradykinin, ATP, histamine, thrombin, acetylcholine and adenosine all evoked a transient hyperpolarization of 10-40 mV lasting 1 min or less, which then turned into a depolarization.8. The K+ channel openers cromakalim (BRL 34915) and lemakalim (BRL 38227) did not affect the membrane potential of GCECs or BAECs. This suggests that ATPsensitive K+ channels are absent in endothelial cells.9. Reducing the oxygen tension (Po2) of the superfusate from 150 mmHg to 12-32 mmHg also had virtually no effect on the resting potential of BAECs and GCECs. However, in sixteen out of twenty-six experiments 15 min hypoxia produced an increase in input resistance; the median of the increase was 9 %. This may be due to partial uncoupling of the cells in the monolayer caused by closure of intercellular ...

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Passive electrical properties and electrogenic sodium transport of cultured guinea‐pig coronary endothelial cells.

Cited by 71 publications

References 28 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.

Effects of vasoactive agonists on the membrane potential of cultured bovine aortic and guinea‐pig coronary endothelium.

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