Features of 4-aminopyridine sensitive outward current observed in single smooth muscle cells from the rabbit pulmonary artery

1987 ◽  
Vol 409 (6) ◽  
pp. 561-568 ◽  
Author(s):  
Kohji Okabe ◽  
Kenji Kitamura ◽  
Hirosi Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Outward Current ◽  
Muscle Cells ◽  
Rabbit Pulmonary Artery

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

2005 ◽  
Vol 289 (4) ◽  
pp. H1551-H1559 ◽  
Author(s):  
Eun A. Ko ◽  
Won Sun Park ◽  
Jae-Hong Ko ◽  
Jin Han ◽  
Nari Kim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Phospholipase C ◽  
Muscle Cells ◽  
Transient Increase ◽  
Rabbit Pulmonary Artery ◽  
Intracellular Ca ◽  
Pulmonary Artery Smooth Muscle ◽  
Sustained Increase

In freshly isolated rabbit pulmonary artery smooth muscle cells, endothelin (ET)-1 induced a transient increase in intracellular Ca2+ concentration ([Ca2+]i) followed by a return to the initial [Ca2+]i. This response was not abolished by the voltage-dependent Ca2+ channel blocker nicardipine or removal of Ca2+ from the bath solution but was inhibited by ryanodine and thapsigargin. This finding suggested that the increase in [Ca2+]i induced by ET-1 was attributable to release of Ca2+ from ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ stores. The transient increase in [Ca2+]i induced by ET-1 was also inhibited by pretreatment with antagonists of ET type A and B (ETA and ETB) receptors (BQ-123 and BQ-788, respectively). Furthermore, the ETB receptor agonist IRL-1620 induced an increase in [Ca2+]i that was followed by a sustained increase in [Ca2+]i; the sustained increase in [Ca2+]i was blocked by nicardipine. Using the nystatin-perforated patch-clamp technique, we found that IRL-1620 caused an increase in Ca2+ current that was inhibited by addition of ET-1. ET-1 did not inhibit Ca2+ 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 [Ca2+]i increases induced by ETB receptor activation. Western blot analysis confirmed expression of ETA and ETB receptors. Finally, U-73122 inhibited the ET-1-induced [Ca2+]i increase, indicating that phospholipase C was involved in modulation of the ET-1-induced [Ca2+]i increase in rabbit pulmonary artery smooth muscle cells.

scholarly journals Calcineurin Aα but Not Aβ Augments ICl(Ca)in Rabbit Pulmonary Artery Smooth Muscle Cells

2004 ◽  
Vol 279 (37) ◽  
pp. 38830-38837 ◽  
Author(s):  
Iain A. Greenwood ◽  
Jonathan Ledoux ◽  
Amy Sanguinetti ◽  
Brian A. Perrino ◽  
Normand Leblanc
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rabbit Pulmonary Artery ◽  
Pulmonary Artery Smooth Muscle

Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells

2002 ◽  
Vol 283 (1) ◽  
pp. L120-L129 ◽  
Author(s):  
Eric Dubuis ◽  
Mathieu Gautier ◽  
Alexandre Melin ◽  
Manuel Rebocho ◽  
Catherine Girardin ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Outward Current ◽  
Muscle Cells ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Whole Cell Patch Clamp

Exogenous carbon monoxide (CO) can induce pulmonary vasodilation by acting directly on pulmonary artery (PA) smooth muscle cells. We investigated the contribution of K+ channels to the regulation of resistance PA resting membrane potential on control (PAC) rats and rats exposed to CO for 3 wk at 530 parts/million, labeled as PACO rats. Whole cell patch-clamp experiments revealed that the resting membrane potential of PACO cells was more negative than that of PAC cells. This was associated with a decrease of membrane resistance in PACO cells. Additional analysis showed that outward current density in PACO cells was higher (50% at +60 mV) than in PAC cells. This was linked to an increase of iberiotoxin (IbTx)-sensitive current. Chronic CO hyperpolarized membrane of pressurized PA from −46.9 ± 1.2 to −56.4 ± 2.6 mV. Additionally, IbTx significantly depolarized membrane of smooth muscle cells from PACO arteries but not from PAC arteries. The present study provides initial evidence of an increase of Ca2+-activated K+ current in smooth muscle cells from PA of rats exposed to chronic CO.

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