scholarly journals Mefenamic acid as a novel activator of L-type voltage-dependent Ca2+ channels in smooth muscle cells from pig proximal urethra

2005 ◽  
Vol 144 (7) ◽  
pp. 919-925 ◽  
Author(s):  
Noriyoshi Teramoto ◽  
Toshihisa Tomoda ◽  
Yushi Ito
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mefenamic Acid ◽  
Muscle Cells ◽  
Voltage Dependent ◽  
Proximal Urethra ◽  
Ca2 Channels

Dual regulation of L-type Ca2+ channels by serotonin 2 receptor stimulation in vascular smooth muscle cells

1995 ◽  
Vol 268 (2) ◽  
pp. H544-H549 ◽  
Author(s):  
Y. Hirakawa ◽  
T. Kuga ◽  
S. Kobayashi ◽  
H. Kanaide ◽  
A. Takeshita
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cell Voltage ◽  
Muscle Cells ◽  
Receptor Stimulation ◽  
Aortic Smooth Muscle ◽  
A 23187 ◽  
Inositol 1,4,5 Trisphosphate ◽  
Voltage Dependent ◽  
Ca2 Channels

The purpose of the present study was to investigate regulation of voltage-dependent Ca2+ channels by serotonin in rat aortic smooth muscle cells in primary culture. L- and T-type Ca2+ currents (ICa) were recorded using the whole cell voltage-clamp method. Without pretreatment, in 25 of 30 cells examined, 10 microM serotonin decreased L-type ICa to various extents (-14 to -72%). However, in the remaining five cells, serotonin increased L-type ICa 21 +/- 4%. Thus, in 30 cells, serotonin decreased L-type ICa an average of 22 +/- 5%. In the presence of intracellular heparin (100 micrograms/ml), a blocker of inositol 1,4,5-trisphosphate binding to its receptor, serotonin increased L-type ICa in all cells 29 +/- 3% (n = 6). When stored Ca2+ was depleted by pretreatment either with 20 microM ryanodine and 20 mM caffeine or with 100 nM A-23187, serotonin also increased L-type ICa in all cells 30 +/- 5 (n = 4) or 37 +/- 5% (n = 12), respectively. In the presence of heparin, the serotonin-induced increase of L-type ICa was prevented by 100 nM staurosporine (2 +/- 3%; n = 6, P < 0.01). The serotonin-induced decrease of L-type ICa was significantly augmented by 100 nM staurosporine (-43 +/- 10%; n = 5). Phorbol 12,13-dibutylate (PDBu; 1 microM) increased L-type ICa 29 +/- 3% (n = 6), and serotonin did not further increase L-type ICa after its potentiation by PDBu.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ethanol (EtOH) inhibits L-type voltage-dependent Ca2+ channels (VDCCs) in bladder smooth muscle cells.

1999 ◽  
Vol 79 ◽  
pp. 274
Author(s):  
Kenji Shirotani ◽  
Atsuo Hara ◽  
Atsuko Higo ◽  
Chihaya Tammi ◽  
Masashi Katsura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Voltage Dependent ◽  
Ca2 Channels

Low PO2 inhibits calcium channel activity in arterial smooth muscle cells

1996 ◽  
Vol 271 (6) ◽  
pp. H2290-H2299 ◽  
Author(s):  
A. Franco-Obregon ◽  
J. Lopez-Barneo
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Pulmonary Arteries ◽  
Muscle Cells ◽  
Channel Activity ◽  
Porcine Coronary Artery ◽  
Voltage Curve ◽  
Voltage Dependent ◽  
Ca2 Channels

We studied the effect of O2 tension (PO2) on the activity of voltage-gated Ca2+ channels recorded in whole cell patch-clamped smooth muscle cells enzymatically dispersed from rabbit cerebral, celiac, femoral, and main pulmonary arteries, as well as from the porcine coronary artery. In all myocyte classes examined, a reduction of PO2 (hypoxia) produced a rapid and reversible inhibition of the macroscopic L-type Ca2+ current of similar general characteristics. The hypoxic inhibition of Ca2+ channel activity closely followed the time course of bath exchange, first becoming apparent at below approximately 80 mmHg PO2. The interaction of O2 with the Ca2+ channels was strongly voltage dependent. At -30 mV the average extent of current inhibition was approximately 80%; however, no effect or even potentiation of current amplitude was observed at potentials more positive than +30 mV. Hypoxia selectively slowed activation kinetics (approximately 1.5 times at -20 mV); however, channel deactivation and inactivation were unaltered by low PO2. In addition, hypoxia produced a reversible shift (8.1 +/- 1.0 mV, n = 12) of the Ca2+ conductance-voltage curve toward positive membrane potentials. We propose that the O2 sensitivity of Ca2+ channels may contribute to the well-known hypoxic dilatation of systemic and the main pulmonary arteries.

Intracellular pH regulates voltage-dependent Ca2+ channels in porcine tracheal smooth muscle cells

1995 ◽  
Vol 268 (4) ◽  
pp. L642-L646 ◽  
Author(s):  
M. Yamakage ◽  
K. S. Lindeman ◽  
C. A. Hirshman ◽  
T. L. Croxton
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Tracheal Smooth Muscle ◽  
Airway Smooth Muscle Cells ◽  
Smooth Muscle Contractility ◽  
Voltage Dependent ◽  
Airway Tone ◽  
Ca2 Channels

Changes in CO2 or in pH modify airway smooth muscle contractility. To investigate the mechanisms involved, we compared K(+)-induced contractions in porcine bronchial rings exposed to different CO2 concentrations and directly measured the effects of changes in intracellular (pHi) or extracellular pH (pHo) on Ca2+ currents (ICa) through voltage-dependent Ca2+ channels (VDC) in porcine tracheal smooth muscle cells. Hypocapnia and hypercapnia caused leftward and rightward shifts, respectively, in the dose-response to K+ (P < 0.05) but did not change the maximum force obtained. Peak ICa (10 mM external Ca2+) elicited by depolarizing pulses from -80 mV was maximal [-265 +/- 12 pA (mean +/- SE), n = 19] at +10 mV. Intracellular acidification decreased the peak ICa at +10 mV from -261 +/- 20 pA to -177 +/- 12 pA (P < 0.05, n = 4), while intracellular alkalinization increased the peak ICa at +10 mV from -302 +/- 27 pA to -368 +/- 26 pA (P < 0.05, n = 4). Changes in pHo had little effect on ICa. There was no shift in the voltage-dependence of induced ICa with any change. We conclude that pHi, but not pHo, directly modulates the entry of Ca2+ into airway smooth muscle cells through VDC. This mechanism may contribute to regulation of airway tone by CO2.

Cholinergic regulation of voltage-dependent Ca2+ channels in porcine tracheal smooth muscle cells

1995 ◽  
Vol 269 (6) ◽  
pp. L776-L782 ◽  
Author(s):  
M. Yamakage ◽  
C. A. Hirshman ◽  
T. L. Croxton
Keyword(s):  
Smooth Muscle ◽  
Charge Carrier ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tracheal Smooth Muscle ◽  
Whole Cell ◽  
Cholinergic Regulation ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Ca2 Channels

To investigate cholinergic regulation of voltage-dependent Ca2+ channels (VDCs) in airway smooth muscle, we measured inward currents through VDCs in enzymatically dispersed porcine tracheal smooth muscle cells using conventional (10 mM Ca2+ as charge carrier) and nystatin-perforated (5 mM Ba2+ as charge carrier) whole cell patch clamp techniques. Carbachol (CCh) had significant and dose-dependent inhibitory effects on inward currents (12% with 10(-7) M and 42% with 10(-6) M) in perforated whole cell clamp experiments, but had no effect on currents in conventional whole cell experiments. CCh also shifted the steady-state inactivation curve to more negative potentials. Further experiments tested the hypothesis that CCh inhibits VDCs in part by the activation of protein kinase C (PKC). Phorbol 12,13-diacetate, an exogenous PKC activator, inhibited currents through VDCs. and calphostin C, a specific PKC inhibitor, antagonized the inhibitory effect of CCh. Furthermore, intracellular exposure to the activating PKC fragment 530-558, using a pipette perfusion technique, also inhibited currents through VDCs. We conclude that cholinergic receptor stimulation can inhibit inward Ca2+ currents through VDCs of porcine tracheal smooth muscle and that this effect may be mediated in part by activation of PKC.

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