Spontaneous electrical rhythmicity and the role of the sarcoplasmic reticulum in the excitability of guinea pig gallbladder smooth muscle cells

2006 ◽  
Vol 290 (4) ◽  
pp. G655-G664 ◽  
Author(s):  
Onesmo B. Balemba ◽  
Matthew J. Salter ◽  
Thomas J. Heppner ◽  
Adrian D. Bonev ◽  
Mark T. Nelson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Action Potentials ◽  
Cyclopiazonic Acid ◽  
Cellular Mechanisms ◽  
Voltage Dependent ◽  
Spontaneous Action ◽  
Potential Activity ◽  
Spontaneous Action Potentials

Spontaneous action potentials and Ca2+ transients were investigated in intact gallbladder preparations to determine how electrical events propagate and the cellular mechanisms that modulate these events. Rhythmic phasic contractions were preceded by Ca2+ flashes that were either focal (limited to one or a few bundles), multifocal (occurring asynchronously in several bundles), or global (simultaneous flashes throughout the field). Ca2+ flashes and action potentials were abolished by inhibiting sarcoplasmic reticulum (SR) Ca2+ release via inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] channels with 2-aminoethoxydiphenyl borate and xestospongin C or by inhibiting voltage-dependent Ca2+ channels (VDCCs) with nifedipine or diltiazem or nisoldipine. Inhibiting ryanodine channels with ryanodine caused multiple spikes superimposed upon plateaus of action potentials and extended quiescent periods. Depletion of SR Ca2+ stores with thapsigargin or cyclopiazonic acid increased the frequency and duration of Ca2+ flashes and action potentials. Acetylcholine, carbachol, or cholecystokinin increased synchronized and increased the frequency of Ca2+ flashes and action potentials. The phospholipase C (PLC) inhibitor U-73122 did not affect Ca2+ flash or action potential activity but inhibited the excitatory effects of acetylcholine on these events. These results indicate that Ca2+ flashes correspond to action potentials and that rhythmic excitation in the gallbladder is multifocal among gallbladder smooth muscle bundles and can be synchronized by excitatory agonists. These events do not depend on PLC activation, but agonist stimulation involves activation of PLC. Generation of these events depends on Ca2+ entry via VDCCs and on Ca2+ mobilization from the SR via Ins(1,4,5)P3 channels.

scholarly journals Acidosis facilitates spontaneous sarcoplasmic reticulum Ca2+ release in rat myocardium.

1987 ◽  
Vol 90 (1) ◽  
pp. 145-165 ◽  
Author(s):  
C H Orchard ◽  
S R Houser ◽  
A A Kort ◽  
A Bahinski ◽  
M C Capogrossi ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potentials ◽  
Laser Light ◽  
De Novo ◽  
Resting Membrane Potential ◽  
Resting Tension ◽  
Spontaneous Action ◽  
The Mean ◽  
Spontaneous Action Potentials ◽  
Tissue Motion

Previous studies have shown that acidosis increases myoplasmic [Ca2+] (Cai). We have investigated whether this facilitates spontaneous sarcoplasmic reticulum (SR) Ca2+ release and its functional sequelae. In unstimulated rat papillary muscles, exposure to an acid solution (produced by increasing the [CO2] of the perfusate from 5 to 20%) caused a rapid increase in the mean tissue Cai, as measured by the photoprotein aequorin. This was paralleled by an increase in spontaneous microscopic tissue motion caused by localized Ca2+ myofilament interactions, as monitored in fluctuations in the intensity of laser light scattered by the muscle. In regularly stimulated muscles, acidosis increased the size of the Ca2+ transient associated with each contraction and caused the appearance of Cai oscillations in the diastolic period. In unstimulated single myocytes, acidosis depolarized the resting membrane potential by approximately 5 mV and enhanced the frequency of spontaneous contractile waves. The small sarcolemmal depolarization associated with each contractile wave increased and occasionally initiated spontaneous action potentials. In regularly stimulated myocytes, acidosis caused de novo spontaneous contractile waves between twitches; these waves were associated with a decrease in the amplitude of the subsequent stimulated twitch. Ryanodine (2 microM) abolished all evidence of spontaneous Ca2+ release during acidosis, markedly reduced the acidosis-induced increase in aequorin light, and reduced resting tension. We conclude that acidosis increases the likelihood for the occurrence of spontaneous SR Ca2+ release, which can cause spontaneous action potentials, increase resting tension, and negatively affect twitch tension.

Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle

2008 ◽  
Vol 294 (2) ◽  
pp. G467-G476 ◽  
Author(s):  
Onesmo B. Balemba ◽  
Aaron C. Bartoo ◽  
Mark T. Nelson ◽  
Gary M. Mawe
Keyword(s):  
Smooth Muscle ◽  
Rhythmic Activity ◽  
Atp Production ◽  
Mitochondrial Inhibitors ◽  
Carbonyl Cyanide ◽  
Spontaneous Action ◽  
Cells Of Cajal ◽  
Spontaneous Action Potentials ◽  
Spontaneous Rhythmic Activity

Mitochondrial Ca2+ handling has been implicated in spontaneous rhythmic activity in smooth muscle and interstitial cells of Cajal. In this investigation we evaluated the effect of mitochondrial inhibitors on spontaneous action potentials (APs), Ca2+ flashes, and Ca2+ waves in gallbladder smooth muscle (GBSM). Disruption of the mitochondrial membrane potential with carbonyl cyanide 3-chlorophenylhydrazone, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone, rotenone, and antimycin A significantly reduced or eliminated APs, Ca2+ flashes, and Ca2+ waves in GBSM. Blockade of ATP production with oligomycin did not alter APs or Ca2+ flashes but significantly reduced Ca2+ wave frequency. Inhibition of mitochondrial Ca2+ uptake and Ca2+ release with Ru360 and CGP-37157, respectively, reduced the frequency of Ca2+ flashes and Ca2+ waves in GBSM. Similar to oligomycin, cyclosporin A did not alter AP and Ca2+ flash frequency but significantly reduced Ca2+ wave activity. These data suggest that mitochondrial Ca2+ handling is necessary for the generation of spontaneous electrical activity and may therefore play an important role in gallbladder tone and motility.

scholarly journals SK Current, Expressed During the Development and Regeneration of Chick Hair Cells, Contributes to the Patterning of Spontaneous Action Potentials

2022 ◽  
Vol 15 ◽  
Author(s):  
Snezana Levic
Keyword(s):  
Electrical Activity ◽  
Hair Cells ◽  
Action Potentials ◽  
Functional Expression ◽  
Basilar Papilla ◽  
Spontaneous Electrical Activity ◽  
Intracellular Ca ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Chick hair cells display calcium (Ca2+)-sensitive spontaneous action potentials during development and regeneration. The role of this activity is unclear but thought to be involved in establishing proper synaptic connections and tonotopic maps, both of which are instrumental to normal hearing. Using an electrophysiological approach, this work investigated the functional expression of Ca2+-sensitive potassium [IK(Ca)] currents and their role in spontaneous electrical activity in the developing and regenerating hair cells (HCs) in the chick basilar papilla. The main IK(Ca) in developing and regenerating chick HCs is an SK current, based on its sensitivity to apamin. Analysis of the functional expression of SK current showed that most dramatic changes occurred between E8 and E16. Specifically, there is a developmental downregulation of the SK current after E16. The SK current gating was very sensitive to the availability of intracellular Ca2+ but showed very little sensitivity to T-type voltage-gated Ca2+ channels, which are one of the hallmarks of developing and regenerating hair cells. Additionally, apamin reduced the frequency of spontaneous electrical activity in HCs, suggesting that SK current participates in patterning the spontaneous electrical activity of HCs.

Actions of histamine on muscle and ganglia of the guinea pig gallbladder

2000 ◽  
Vol 279 (3) ◽  
pp. G622-G630 ◽  
Author(s):  
Jason M. Hemming ◽  
Fay A. Guarraci ◽  
Tracy A. Firth ◽  
Lee J. Jennings ◽  
Mark T. Nelson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Mast Cells ◽  
Action Potentials ◽  
Resting Membrane Potential ◽  
Receptor Subtype ◽  
Excitatory Postsynaptic Potential ◽  
Membrane Hyperpolarization ◽  
Spontaneous Action ◽  
Induced Changes ◽  
Spontaneous Action Potentials

Histamine is an inflammatory mediator present in mast cells, which are abundant in the wall of the gallbladder. We examined the electrical properties of gallbladder smooth muscle and nerve associated with histamine-induced changes in gallbladder tone. Recordings were made from gallbladder smooth muscle and neurons, and responses to histamine and receptor subtype-specific compounds were tested. Histamine application to intact smooth muscle produced a concentration-dependent membrane depolarization and increased excitability. In the presence of the H2 antagonist ranitidine, the response to histamine was potentiated. Activation of H2 receptors caused membrane hyperpolarization and elimination of spontaneous action potentials. The H2response was attenuated by the ATP-sensitive K+(KATP) channel blocker glibenclamide in intact and isolated smooth muscle. Histamine had no effect on the resting membrane potential or excitability of gallbladder neurons. Furthermore, neither histamine nor the H3 agonist R-α-methylhistamine altered the amplitude of the fast excitatory postsynaptic potential in gallbladder ganglia. The mast cell degranulator compound 48/80 caused a smooth muscle depolarization that was inhibited by the H1 antagonist mepyramine, indicating that histamine released from mast cells can activate gallbladder smooth muscle. In conclusion, histamine released from mast cells can act on gallbladder smooth muscle, but not in ganglia. The depolarization and associated contraction of gallbladder smooth muscle represent the net effect of activation of both H1 (excitatory) and H2 (inhibitory) receptors, with the H2receptor-mediated response involving the activation of KATPchannels.

scholarly journals Minor role of a Ca2+-depleted sarcoplasmic reticulum in heterologous desensitization of smooth muscle to K+

1998 ◽  
Vol 275 (4) ◽  
pp. C1095-C1103 ◽  
Author(s):  
Robert L. Wardle ◽  
Richard A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Cyclopiazonic Acid ◽  
Minor Role ◽  
Large Reduction ◽  
Atpase Inhibitor ◽  
Before And After ◽  
Heterologous Desensitization ◽  
Porcine Carotid Artery

Exposure of porcine carotid artery smooth muscle (PCASM) to histamine was followed by a large reduction in the rate of force generation in response to 40 mM KCl. This was shown to be a manifestation of slow attainment of a steady-state myoplasmic Ca2+concentration ([Ca2+]i). We hypothesized that if net transsarcolemmal Ca2+ flux into the depolarized PCASM cells is the same before and after a desensitizing histamine treatment, then the transient attenuation of the increase in [Ca2+]imay be due to accelerated uptake of Ca2+ by a partially depleted sarcoplasmic reticulum (SR) acting as a Ca2+ sink or superficial buffer barrier. We tested this hypothesis by eliciting responses of “desensitized PCASM” to 40 mM KCl in the presence of cyclopiazonic acid (CPA), an SR Ca2+-ATPase inhibitor. Contractions of CPA-treated tissues were attenuated less than those of tissues not treated with CPA, but they were not abolished. CPA-insensitive mechanism(s) dominated the desensitization. We conclude that histamine pretreatment reduced net transsarcolemmal Ca2+ flux into PCASM in response to 40 mM KCl.

Cholesterol inhibits spontaneous action potentials and calcium currents in guinea pig gallbladder smooth muscle

1999 ◽  
Vol 277 (5) ◽  
pp. G1017-G1026 ◽  
Author(s):  
Lee J. Jennings ◽  
Qi-Wei Xu ◽  
Tracy A. Firth ◽  
Mark T. Nelson ◽  
Gary M. Mawe
Keyword(s):  
Smooth Muscle ◽  
Action Potentials ◽  
Second Messenger ◽  
Calcium Currents ◽  
Isolated Cells ◽  
Receptor Ligand ◽  
Intact Tissue ◽  
Elevated Cholesterol ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Elevated cholesterol decreases agonist-induced contractility and enhances stone formation in the gallbladder. The current study was conducted to determine if and how the electrical properties and ionic conductances of gallbladder smooth muscle are altered by elevated cholesterol. Cholesterol was delivered as a complex with cyclodextrin, and effects were evaluated with intracellular recordings from intact gallbladder and whole cell patch-clamp recordings from isolated cells. Cholesterol significantly attenuated the spontaneous action potentials of intact tissue. Furthermore, calcium-dependent action potentials and calcium currents were reduced in the intact tissue and in isolated cells, respectively. However, neither membrane potential hyperpolarizations induced by the ATP-sensitive potassium channel opener, pinacidil, nor voltage-activated outward potassium currents were affected by cholesterol. Hyperpolarizations elicited by calcitonin gene-related peptide were reduced by cholesterol enrichment, indicating potential changes in receptor ligand binding and/or second messenger interactions. These data indicate that excess cholesterol can contribute to gallbladder stasis by affecting calcium channel activity, whereas potassium channels remained unaffected. In addition, cholesterol enrichment may also modulate receptor ligand behavior and/or second messenger interactions.

Role of K+ Channels in Frequency Regulation of Spontaneous Action Potentials in Rat Pituitary GH3 Cells

2003 ◽  
Vol 78 (5) ◽  
pp. 260-269 ◽  
Author(s):  
Suk-Ho Lee ◽  
Eun Hae Lee ◽  
Shin Young Ryu ◽  
Hyewhon Rhim ◽  
Hye-Jung Baek ◽  
...  
Keyword(s):  
Action Potentials ◽  
Frequency Regulation ◽  
Rat Pituitary ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Vascular muscle cell depolarization and activation in renal arteries on elevation of transmural pressure

1987 ◽  
Vol 253 (4) ◽  
pp. F778-F781 ◽  
Author(s):  
D. R. Harder ◽  
R. Gilbert ◽  
J. H. Lombard
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Cell ◽  
Action Potentials ◽  
Transmural Pressure ◽  
Renal Arteries ◽  
Resting Potential ◽  
Internal Diameter ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

The goal of this study was to define some of the cellular and ionic mechanisms of smooth muscle cell activation in dog renal arteries exposed to physiological levels of transmural pressure. Isolated interlobular arteries were cannulated and connected to a pressure reservoir to allow manipulation of transmural pressure in 20-mmHg increment steps from 20 to 120 mmHg. As transmural pressure was increased, vascular smooth muscle exhibited a linear depolarization from an average resting potential of -57+/- 2 mV at 20 mmHg to -38+/- 2.4 mV at 120 mmHg. Spontaneous action potentials could often be recorded at pressures greater than 80 mmHg. These appeared to occur primarily at bifurcation points of branching arteries. Vascular smooth muscle depolarization and action potentials occurring in response to increases in transmural pressure were associated with a maintenance of internal diameter of the vessel segments despite increases in transmural pressure in the range between 60 and 120 mmHg. The “pressure-induced” activation of vascular smooth muscle contraction and spontaneous action potentials of small renal arteries at higher transmural pressures were blocked on Ca2+ channel inhibition with verapamil (10(-6) M). These data document a membrane ionic mechanism (probably increased Ca2+ influx) for pressure-induced myogenic activation of isolated renal arteries. It is interesting that the contraction of these vessels occurs over the pressure range in which autoregulation of renal blood flow normally occurs. The physiological significance of these responses needs to be determined.

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