Electrical behavior of guinea pig tracheal smooth muscle

2000 ◽  
Vol 278 (2) ◽  
pp. L320-L328 ◽  
Author(s):  
Narelle J. Bramich
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Nerve Stimulation ◽  
Tracheal Smooth Muscle ◽  
Quiescent Cells ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Intrinsic Nerve ◽  
Spontaneous Oscillations

Intracellular recordings were taken from the smooth muscle of the guinea pig trachea, and the effects of intrinsic nerve stimulation were examined. Approximately 50% of the cells had stable resting membrane potentials of −50 ± 1 mV. The remaining cells displayed spontaneous oscillations in membrane potential, which were abolished either by blocking voltage-dependent Ca2+channels with nifedipine or by depleting intracellular Ca2+stores with ryanodine. In quiescent cells, stimulation with a single impulse evoked an excitatory junction potential (EJP). In 30% of these cells, trains of stimuli evoked an EJP that was followed by oscillations in membrane potential. Transmural nerve stimulation caused an increase in the frequency of spontaneous oscillations. All responses were abolished by the muscarinic-receptor antagonist hyoscine (1 μM). In quiescent cells, nifedipine (1 μM) reduced EJPs by 30%, whereas ryanodine (10 μM) reduced EJPs by 93%. These results suggest that both the release of Ca2+ from intracellular stores and the influx of Ca2+ through voltage-dependent Ca2+channels are important determinants of spontaneous and nerve-evoked electrical activity of guinea pig tracheal smooth muscle.

Na+/Ca2+ exchange and its role in intracellular Ca2+ regulation in guinea pig detrusor smooth muscle

2001 ◽  
Vol 280 (5) ◽  
pp. C1090-C1096 ◽  
Author(s):  
C. Wu ◽  
C. H. Fry
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Outward Current ◽  
Detrusor Smooth Muscle ◽  
Small Rise ◽  
Intracellular Ca ◽  
Net Flux ◽  
Isolated Smooth Muscle Cells

The role of Na+/Ca2+ exchange in regulating intracellular Ca2+ concentration ([Ca2+]i) in isolated smooth muscle cells from the guinea pig urinary bladder was investigated. Incremental reduction of extracellular Na+ concentration resulted in a graded rise of [Ca2+]i; 50–100 μM strophanthidin also increased [Ca2+]i. A small outward current accompanied the rise of [Ca2+]i in low-Na+ solutions (17.1 ± 1.8 pA in 29.4 mM Na+). The quantity of Ca2+ influx through the exchanger was estimated from the charge carried by the outward current and was ∼30 times that which is necessary to account for the rise of [Ca2+]i, after correction was made for intracellular Ca2+ buffering. Ca2+ influx through the exchanger was able to load intracellular Ca2+ stores. It is concluded that the level of resting [Ca2+]i is not determined by the exchanger, and under resting conditions (membrane potential −50 to −60 mV), there is little net flux through the exchanger. However, a small rise of intracellular Na+ concentration would be sufficient to generate significant net Ca2+ influx.

ω-3 Polyunsaturated fatty acids—modulation of voltage-dependent L-type Ca2+ current in guinea-pig tracheal smooth muscle cells

1998 ◽  
Vol 355 (2-3) ◽  
pp. 257-266 ◽  
Author(s):  
Hisanori Hazama ◽  
Toshiaki Nakajima ◽  
Michiko Asano ◽  
Kuniaki Iwasawa ◽  
Toshihiro Morita ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Guinea Pig ◽  
Polyunsaturated Fatty Acids ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tracheal Smooth Muscle ◽  
Voltage Dependent

Ion channels in smooth muscle: regulators of intracellular calcium and contractility

2005 ◽  
Vol 83 (3) ◽  
pp. 215-242 ◽  
Author(s):  
Kevin S Thorneloe ◽  
Mark T Nelson
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Membrane Potential ◽  
Ion Channels ◽  
Feedback Mechanism ◽  
Negative Feedback Mechanism ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Active Channels ◽  
Trisphosphate Receptor

Smooth muscle (SM) is essential to all aspects of human physiology and, therefore, key to the maintenance of life. Ion channels expressed within SM cells regulate the membrane potential, intracellular Ca2+ concentration, and contractility of SM. Excitatory ion channels function to depolarize the membrane potential. These include nonselective cation channels that allow Na+ and Ca2+ to permeate into SM cells. The nonselective cation channel family includes tonically active channels (Icat), as well as channels activated by agonists, pressure-stretch, and intracellular Ca2+ store depletion. Cl--selective channels, activated by intracellular Ca2+ or stretch, also mediate SM depolarization. Plasma membrane depolarization in SM activates voltage-dependent Ca2+ channels that demonstrate a high Ca2+ selectivity and provide influx of contractile Ca2+. Ca2+ is also released from SM intracellular Ca2+ stores of the sarcoplasmic reticulum (SR) through ryanodine and inositol trisphosphate receptor Ca2+ channels. This is part of a negative feedback mechanism limiting contraction that occurs by the Ca2+-dependent activation of large-conductance K+ channels, which hyper polarize the plasma membrane. Unlike the well-defined contractile role of SR-released Ca2+ in skeletal and cardiac muscle, the literature suggests that in SM Ca2+ released from the SR functions to limit contractility. Depolarization-activated K+ chan nels, ATP-sensitive K+ channels, and inward rectifier K+ channels also hyperpolarize SM, favouring relaxation. The expression pattern, density, and biophysical properties of ion channels vary among SM types and are key determinants of electrical activity, contractility, and SM function.Key words: smooth muscle, ion channel, membrane potential, calcium, contraction.

Cyclopiazonic acid decreases spontaneous transient depolarizations in guinea pig mesenteric lymphatic vessels in endothelium-dependent and -independent manners

2004 ◽  
Vol 286 (6) ◽  
pp. H2287-H2295 ◽  
Author(s):  
Ilia Ferrusi ◽  
Jun Zhao ◽  
Dirk van Helden ◽  
Pierre-Yves von der Weid
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Lymphatic Vessels ◽  
Cyclopiazonic Acid ◽  
Muscle Membrane ◽  
Pacemaker Activity ◽  
Smooth Muscle Membrane ◽  
Intracellular Ca

Guinea pig mesenteric lymphatic vessels exhibit vasomotion through a pacemaker mechanism that involves intracellular Ca2+ release and resultant spontaneous transient depolarizations (STDs) of the smooth muscle membrane potential. This study presents a detailed characterization of the effects of cyclopiazonic acid (CPA) on this pacemaker activity. Microelectrode recordings from smooth muscle in vessel segments revealed that application of CPA (1–10 μM) caused a hyperpolarization accompanied by a decrease in the frequency and amplitude of STDs. The CPA-induced hyperpolarization was abolished after destruction of the endothelium and in the presence of NG-nitro-l-arginine (100 μM) or 1 H-[1,2,4]oxadiazolol-[4,3- a]quinoxaline-1-one (10 μM), which suggests a contribution of endothelium-derived nitric oxide (EDNO) in this response. In the absence of EDNO-induced effects, CPA decreased the frequency and amplitude of STDs recorded before and in the presence of the thromboxane A2 mimetic U-46619, norepinephrine, or thimerosal. CPA abolished U-46619-induced vasomotion as determined by measurement of constriction-associated intracellular Ca2+ concentration using the ratiometric Ca2+ indicator fura-2. The endothelial actions of CPA were compared with those of ACh, which is known to cause EDNO release in this preparation. Although CPA and ACh both increased endothelial intracellular Ca2+ concentration and depolarized the membrane potential, the kinetics of action for both parameters were markedly slower for CPA than ACh. These results suggest that CPA first hyperpolarizes the lymphatic smooth muscle and decreases STD frequency and amplitude through endothelial release of EDNO, and second, consistent with the action of CPA to inhibit sarcoplasmic reticulum Ca2+-ATPase and deplete Ca2+ stores, it further reduces STD activity. Inhibition of the lymphatic smooth muscle pacemaker mechanism is thought to abolish agonist-induced vasomotion.

Calcium sparks in smooth muscle

2000 ◽  
Vol 278 (2) ◽  
pp. C235-C256 ◽  
Author(s):  
Jonathan H. Jaggar ◽  
Valerie A. Porter ◽  
W. Jonathan Lederer ◽  
Mark T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Negative Feedback ◽  
Muscle Function ◽  
Feedback Regulation ◽  
Smooth Muscle Contractility ◽  
Negative Feedback Regulation ◽  
Smooth Muscle Function ◽  
Voltage Dependent ◽  
Intracellular Ca

Local intracellular Ca2+transients, termed Ca2+ sparks, are caused by the coordinated opening of a cluster of ryanodine-sensitive Ca2+ release channels in the sarcoplasmic reticulum of smooth muscle cells. Ca2+ sparks are activated by Ca2+ entry through dihydropyridine-sensitive voltage-dependent Ca2+ channels, although the precise mechanisms of communication of Ca2+ entry to Ca2+ spark activation are not clear in smooth muscle. Ca2+ sparks act as a positive-feedback element to increase smooth muscle contractility, directly by contributing to the global cytoplasmic Ca2+ concentration ([Ca2+]) and indirectly by increasing Ca2+ entry through membrane potential depolarization, caused by activation of Ca2+ spark-activated Cl− channels. Ca2+ sparks also have a profound negative-feedback effect on contractility by decreasing Ca2+ entry through membrane potential hyperpolarization, caused by activation of large-conductance, Ca2+-sensitive K+ channels. In this review, the roles of Ca2+sparks in positive- and negative-feedback regulation of smooth muscle function are explored. We also propose that frequency and amplitude modulation of Ca2+ sparks by contractile and relaxant agents is an important mechanism to regulate smooth muscle function.

scholarly journals Large-conductance voltage- and Ca2+-activated K+ channel regulation by protein kinase C in guinea pig urinary bladder smooth muscle

2014 ◽  
Vol 306 (5) ◽  
pp. C460-C470 ◽  
Author(s):  
Kiril L. Hristov ◽  
Amy C. Smith ◽  
Shankar P. Parajuli ◽  
John Malysz ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Bk Channels ◽  
Bk Channel ◽  
K Channel ◽  
Channel Activity ◽  
Open Probability ◽  
Channel Regulation ◽  
Pkc Activation

Large-conductance voltage- and Ca2+-activated K+ (BK) channels are critical regulators of detrusor smooth muscle (DSM) excitability and contractility. PKC modulates the contraction of DSM and BK channel activity in non-DSM cells; however, the cellular mechanism regulating the PKC-BK channel interaction in DSM remains unknown. We provide a novel mechanistic insight into BK channel regulation by PKC in DSM. We used patch-clamp electrophysiology, live-cell Ca2+ imaging, and functional studies of DSM contractility to elucidate BK channel regulation by PKC at cellular and tissue levels. Voltage-clamp experiments showed that pharmacological activation of PKC with PMA inhibited the spontaneous transient BK currents in native freshly isolated guinea pig DSM cells. Current-clamp recordings revealed that PMA significantly depolarized DSM membrane potential and inhibited the spontaneous transient hyperpolarizations in DSM cells. The PMA inhibitory effects on DSM membrane potential were completely abolished by the selective BK channel inhibitor paxilline. Activation of PKC with PMA did not affect the amplitude of the voltage-step-induced whole cell steady-state BK current or the single BK channel open probability (recorded in cell-attached mode) upon inhibition of all major Ca2+ sources for BK channel activation with thapsigargin, ryanodine, and nifedipine. PKC activation with PMA elevated intracellular Ca2+ levels in DSM cells and increased spontaneous phasic and nerve-evoked contractions of DSM isolated strips. Our results support the concept that PKC activation leads to a reduction of BK channel activity in DSM via a Ca2+-dependent mechanism, thus increasing DSM contractility.

scholarly journals l-NG-nitro arginine inhibits non-adrenergic, non-cholinergic relaxations of guinea-pig isolated tracheal smooth muscle

1990 ◽  
Vol 100 (4) ◽  
pp. 663-664 ◽  
Author(s):  
John F. Tucker ◽  
Sandra R. Brave ◽  
Litsa Charalambous ◽  
Adrian J. Hobbs ◽  
Alan Gibson
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Tracheal Smooth Muscle

Functional coupling between the Na+/Ca2+ exchanger and nonselective cation channels during histamine stimulation in guinea pig tracheal smooth muscle

2007 ◽  
Vol 293 (1) ◽  
pp. L191-L198 ◽  
Author(s):  
Paola Algara-Suárez ◽  
Catalina Romero-Méndez ◽  
Tom Chrones ◽  
Sergio Sánchez-Armass ◽  
Ulises Meza ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Force Measurement ◽  
Isometric Force ◽  
Sustained Response ◽  
Functional Coupling ◽  
Channel Activation ◽  
Histamine Stimulation ◽  
Nonselective Cation Channels ◽  
Intracellular Ca

Airway smooth muscle (ASM) contracts partly due to an increase in cytosolic Ca2+. In this work, we found that the contraction caused by histamine depends on external Na+, possibly involving nonselective cationic channels (NSCC) and the Na+/Ca2+ exchanger (NCX). We performed various protocols using isometric force measurement of guinea pig tracheal rings stimulated by histamine. We observed that force reached 53 ± 1% of control during external Na+ substitution by N-methyl-d-glucamine+, whereas substitution by Li+ led to no significant change (91 ± 1%). Preincubation with KB-R7943 decreased the maximal force developed (52.3 ± 5.6%), whereas preincubation with nifedipine did not (89.7 ± 1.8%). Also, application of the nonspecific NCX blocker KB-R7943 and nifedipine on histamine-precontracted tracheal rings reduced force to 1 ± 3%, significantly different from nifedipine alone (49 ± 6%). Moreover, nonspecific NSCC inhibitors SKF-96365 and 2-aminoethyldiphenyl borate reduced force to 1 ± 1% and 19 ± 7%, respectively. Intracellular Ca2+ measurements in isolated ASM cells showed that KB-R7943 and SKF-96365 reduced the peak and sustained response to histamine (0.20 ± 0.1 and 0.19 ± 0.09 for KB-R, 0.43 ± 0.16 and 0.47 ± 0.18 for SKF, expressed as mean of differences). Moreover, Na+-free solution only inhibited the sustained response (0.54 ± 0.25). These data support an important role for NSCC and NCX during histamine stimulation. We speculate that histamine induces Na+ influx through NSCC that promotes the Ca2+ entry mode of NCX and CaV1.2 channel activation, thereby causing contraction.

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