G-Protein Regulation of an L-Type Calcium Channel Current in Canine Jejunal Circular Smooth Muscle

1997 ◽  
Vol 160 (1) ◽  
pp. 39-46 ◽  
Author(s):  
G. Farrugia
Keyword(s):  
Smooth Muscle ◽  
Calcium Channel ◽  
G Protein ◽  
Protein Regulation ◽  
Circular Smooth Muscle ◽  
Channel Current

G-protein modulation of Ca2+-activated K+ channels from colon circular smooth muscle

1992 ◽  
Vol 103 (4) ◽  
pp. 1390
Author(s):  
C.L. Gentry ◽  
A.L. Percival ◽  
K.M. Sanders ◽  
A. Carl ◽  
J.L. Kenyon
Keyword(s):  
Smooth Muscle ◽  
G Protein ◽  
K Channels ◽  
Circular Smooth Muscle

Abstract 2622: Serotonin And Endothelin Increase L-type Calcium Channel Current In Pulmonary Artery Smooth Muscle Cells, Unrelated To Changes In Membrane Potential

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Zhigang Hong ◽  
Jesus A Cabrera ◽  
Mohan Dutt ◽  
Basel Aloul ◽  
E. K Weir
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Calcium Channel ◽  
Calcium Current ◽  
Calcium Influx ◽  
Muscle Cells ◽  
Membrane Depolarization ◽  
Channel Current ◽  
Relationship Of

Serotonin (5-HT) and endothelin (ET-1) are both involved in the pathophysiology of idiopathic pulmonary arterial hypertension. In addition to the release of calcium (Ca ++ ) from the internal stores in the smooth muscle cells (SMCs), these agents stimulate entry of Ca ++ through the L-type Ca ++ channel. In isolated rat pulmonary resistance artery (PA) rings, 5-HT (10 μM) caused a contraction of 110 ± 14 % of the contraction elicited by 60 mM KCl. After inhibition of K V and K Ca channels by 4-AP and TEA, 5-HT caused a stronger contraction of 176 ± 4% (p<0.01). Consequently, we studied the relationship of 5-HT- stimulated contraction to membrane potential (E m ) and L-type calcium current in rat resistance PASMCs. Contrary to expectation, 5-HT (1, 10, 100 μM) had no effect on I K or E m (n=5 for each). However, 5-HT (10 μM) increased L-type calcium current between E m -20 and +30 mV (n=7). This effect was inhibited by a PKC blocker (BIS-1, 3 μM), which also caused a marked reduction of 5-HT-stimulated contraction of PA rings (>70% decrease at 10 μM 5-HT). In contrast to 5-HT, ET-1 (10 nM) reduced I K and caused membrane depolarization (from −41 ± 5 to −31 ± 3 mV, n=4). In addition to this effect, ET-1, like 5-HT, increased L-type calcium current over the same range of E m (n=7). This increase was inhibited by nifedipine (3 μM). These experiments indicate that both 5-HT and ET-1 increase calcium influx through the L-type calcium channel in a manner independent of E m . ET-1 has an additional effect of causing membrane depolarization, which also increases calcium entry through L-type channels by altering voltage gating of the channel.

Whole cell current and membrane potential regulation by a human smooth muscle mechanosensitive calcium channel

2000 ◽  
Vol 279 (6) ◽  
pp. G1155-G1161 ◽  
Author(s):  
Adrian N. Holm ◽  
Adam Rich ◽  
Michael G. Sarr ◽  
Gianrico Farrugia
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Outward Current ◽  
Muscle Cells ◽  
Membrane Hyperpolarization ◽  
Whole Cell ◽  
Circular Smooth Muscle ◽  
Channel Current ◽  
Cell Current

Mechanotransduction is required for a wide variety of biological functions. The aim of this study was to determine the effect of activation of a mechanosensitive Ca2+ channel, present in human jejunal circular smooth muscle cells, on whole cell currents and on membrane potential. Currents were recorded using patch-clamp techniques, and perfusion of the bath (10 ml/min, 30 s) was used to mechanoactivate the L-type Ca2+ channel. Perfusion resulted in activation of L-type Ca2+ channels and an increase in outward current from 664 ± 57 to 773 ± 72 pA at +60 mV. Membrane potential hyperpolarized from −42 ± 4 to −50 ± 5 mV. In the presence of nifedipine (10 μM), there was no increase in outward current or change in membrane potential with perfusion. In the presence of charybdotoxin or iberiotoxin, perfusion of the bath did not increase outward current or change membrane potential. A model is proposed in which mechanoactivation of an L-type Ca2+ channel current in human jejunal circular smooth muscle cells results in increased Ca2+ entry and cell contraction. Ca2+ entry activates large-conductance Ca2+-activated K+channels, resulting in membrane hyperpolarization and relaxation.

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