Contractile Agonists Preferentially Activate CL−over K+Currents in Arterial Myocytes

Bakhramov, A.; Hartley, S. Anthony; Salter, Katie J.; Kozlowski, Roland Z.

doi:10.1006/bbrc.1996.1484

Cited by 28 publications

(24 citation statements)

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“…Our results revealed patterns of changes in [Ca 2ϩ ] i that are distinct from those reported elsewhere. For example, ET-1 was reported to induce a large transient [Ca 2ϩ ] i increase followed by a sustained plateau that remained elevated above baseline (8,34), and other studies reported oscillations in [Ca 2ϩ ] i in smooth muscle cells in response to ET-1 (3,16). This discrepancy is most likely attributable to differences in the wide variety of models used to study Ca 2ϩ regulation, which include freshly isolated cells, cultured cells, and different cell types.…”

Section: Discussionmentioning

confidence: 86%

Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C

Ko¹,

Park²,

Ko³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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In freshly isolated rabbit pulmonary artery smooth muscle cells, endothelin (ET)-1 induced a transient increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) followed by a return to the initial [Ca(2+)](i). This response was not abolished by the voltage-dependent Ca(2+) channel blocker nicardipine or removal of Ca(2+) from the bath solution but was inhibited by ryanodine and thapsigargin. This finding suggested that the increase in [Ca(2+)](i) induced by ET-1 was attributable to release of Ca(2+) from ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca(2+) stores. The transient increase in [Ca(2+)](i) induced by ET-1 was also inhibited by pretreatment with antagonists of ET type A and B (ET(A) and ET(B)) receptors (BQ-123 and BQ-788, respectively). Furthermore, the ET(B) receptor agonist IRL-1620 induced an increase in [Ca(2+)](i) that was followed by a sustained increase in [Ca(2+)](i); the sustained increase in [Ca(2+)](i) was blocked by nicardipine. Using the nystatin-perforated patch-clamp technique, we found that IRL-1620 caused an increase in Ca(2+) current that was inhibited by addition of ET-1. ET-1 did not inhibit Ca(2+) current when cells were pretreated with BQ-123. These results suggested that when both receptor types are activated, the opposing responses lead to abolition of the sustained [Ca(2+)](i) increases induced by ET(B) receptor activation. Western blot analysis confirmed expression of ET(A) and ET(B) receptors. Finally, U-73122 inhibited the ET-1-induced [Ca(2+)](i) increase, indicating that phospholipase C was involved in modulation of the ET-1-induced [Ca(2+)](i) increase in rabbit pulmonary artery smooth muscle cells.

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Section: Discussionmentioning

confidence: 86%

Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C

Ko¹,

Park²,

Ko³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…SA). Under these conditions ET-l does not produce notable activation of KCa channels (Bakhramov et al 1996). In contrast, PGF2c (50 AM; in solution C), also known to constrict pulmonary arterial smooth muscle (Xu et al 1995), had no effect on the Em.…”

Section: Synergism Between Depolarization and Hypoxiamentioning

confidence: 78%

“…A typical time course for this effect is shown in Fig. 1 (Salter, Turner, Albarwani, Clapp & Kozlowski, 1995;Bakhramov, Salter, Hartley & Kozlowski, 1996; and others (Brayden & Nelson, 1992) to verify the presence of Kca channel activity. IK was virtually insensitive to IBTX (1-100 nM) at a test potential of +30 mV in the perforated-patch recording configuration (Fig.…”

Section: Initiation Of Hypoxiamentioning

confidence: 85%

Relationship between membrane potential, delayed rectifier K+ currents and hypoxia in rat pulmonary arterial myocytes

Turner

Kozlowski²

1997

Experimental Physiology

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“…A likely candidate would be a Ca 2+ ‐activated Cl − current. Coupling of oscillatory Ca 2+ release to activation of a Cl − channel has been shown in several smooth muscle preparations (Bakhramov et al ., 1996; Liu & Farley, 1996b; Hyvelin et al ., 1998), and in swine tracheal SMCs, it was shown that a tonic increase of IP 3 could induce such oscillations (Liu & Farley, 1996a). The Ca 2+ ‐activated Cl − channels have not been characterized in the same detail as the voltage‐dependent anion channels or the cation channels.…”

Section: Synchronizationmentioning

confidence: 99%

Vasomotion: cellular background for the oscillator and for the synchronization of smooth muscle cells

Aalkjær

Nilsson

2005

British J Pharmacology

166

175

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1 Vasomotion is the oscillation of vascular tone with frequencies in the range from 1 to 20 min À1 seen in most vascular beds. The oscillation originates in the vessel wall and is seen both in vivo and in vitro.2 Recently, our ideas on the cellular mechanisms responsible for vasomotion have improved. Three different types of cellular oscillations have been suggested. One model has suggested that oscillatory release of Ca 2 þ from intracellular stores is important (the oscillation is based on a cytosolic oscillator). A second proposed mechanism is an oscillation originating in the sarcolemma (a membrane oscillator). A third mechanism is based on an oscillation of glycolysis (metabolic oscillator). For the two latter mechanisms, only limited experimental evidence is available. 3 To understand vasomotion, it is important to understand how the cells synchronize. For the cytosolic oscillators synchronization may occur via activation of Ca 2 þ -sensitive ion channels by oscillatory Ca 2 þ release. The ensuing membrane potential oscillation feeds back on the intracellular Ca 2 þ stores and causes synchronization of the Ca 2 þ release. While membrane oscillators in adjacent smooth muscle cells could be synchronized through the same mechanism that sets up the oscillation in the individual cells, a mechanism to synchronize the metabolic-based oscillators has not been suggested. 4 The interpretation of the experimental observations is supported by theoretical modelling of smooth muscle cells behaviour, and the new insight into the mechanisms of vasomotion has the potential to provide tools to investigate the physiological role of vasomotion.

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Contractile Agonists Preferentially Activate CL−over K+Currents in Arterial Myocytes

Cited by 28 publications

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Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C

Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C

Relationship between membrane potential, delayed rectifier K+ currents and hypoxia in rat pulmonary arterial myocytes

Vasomotion: cellular background for the oscillator and for the synchronization of smooth muscle cells

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Contractile Agonists Preferentially Activate CL−over K+Currents in Arterial Myocytes

Cited by 28 publications

References 0 publications

Endothelin-1 increases intracellular Ca2+in rabbit pulmonary artery smooth muscle cells through phospholipase C

Endothelin-1 increases intracellular Ca2+in rabbit pulmonary artery smooth muscle cells through phospholipase C

Relationship between membrane potential, delayed rectifier K+ currents and hypoxia in rat pulmonary arterial myocytes

Vasomotion: cellular background for the oscillator and for the synchronization of smooth muscle cells

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Product

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Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C

Endothelin-1 increases intracellular Ca²⁺in rabbit pulmonary artery smooth muscle cells through phospholipase C