scholarly journals Role of membrane potential in endothelium-dependent relaxation of guinea-pig coronary arterial smooth muscle.

1995 ◽  
Vol 484 (2) ◽  
pp. 469-480 ◽  
Author(s):  
H C Parkington ◽  
M A Tonta ◽  
H A Coleman ◽  
M Tare
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Arterial Smooth Muscle ◽  
Endothelium Dependent Relaxation

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.

Role of calcium in endothelium-dependent relaxation of arterial smooth muscle

1987 ◽  
Vol 59 (2) ◽  
pp. A35-A43 ◽  
Author(s):  
Michael J. Peach ◽  
Harold A. Singer ◽  
Nicholas J. Izzo ◽  
Alex L. Loeb
Keyword(s):  
Smooth Muscle ◽  
Arterial Smooth Muscle ◽  
Endothelium Dependent Relaxation

scholarly journals Kv2.1 channels play opposing roles in regulating membrane potential, Ca2+ channel function, and myogenic tone in arterial smooth muscle

2020 ◽  
Vol 117 (7) ◽  
pp. 3858-3866 ◽  
Author(s):  
Samantha C. O’Dwyer ◽  
Stephanie Palacio ◽  
Collin Matsumoto ◽  
Laura Guarina ◽  
Nicholas R. Klug ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Myogenic Tone ◽  
Arterial Smooth Muscle ◽  
Membrane Hyperpolarization ◽  
Intracellular Ca ◽  
Specific Regulation

The accepted role of the protein Kv2.1 in arterial smooth muscle cells is to form K+ channels in the sarcolemma. Opening of Kv2.1 channels causes membrane hyperpolarization, which decreases the activity of L-type CaV1.2 channels, lowering intracellular Ca2+ ([Ca2+]i) and causing smooth muscle relaxation. A limitation of this model is that it is based exclusively on data from male arterial myocytes. Here, we used a combination of electrophysiology as well as imaging approaches to investigate the role of Kv2.1 channels in male and female arterial myocytes. We confirmed that Kv2.1 plays a canonical conductive role but found it also has a structural role in arterial myocytes to enhance clustering of CaV1.2 channels. Less than 1% of Kv2.1 channels are conductive and induce membrane hyperpolarization. Paradoxically, by enhancing the structural clustering and probability of CaV1.2–CaV1.2 interactions within these clusters, Kv2.1 increases Ca2+ influx. These functional impacts of Kv2.1 depend on its level of expression, which varies with sex. In female myocytes, where expression of Kv2.1 protein is higher than in male myocytes, Kv2.1 has conductive and structural roles. Female myocytes have larger CaV1.2 clusters, larger [Ca2+]i, and larger myogenic tone than male myocytes. In contrast, in male myocytes, Kv2.1 channels regulate membrane potential but not CaV1.2 channel clustering. We propose a model in which Kv2.1 function varies with sex: in males, Kv2.1 channels control membrane potential but, in female myocytes, Kv2.1 plays dual electrical and CaV1.2 clustering roles. This contributes to sex-specific regulation of excitability, [Ca2+]i, and myogenic tone in arterial myocytes.

ERG K+ channels modulate the electrical and contractile activities of gallbladder smooth muscle

2003 ◽  
Vol 284 (3) ◽  
pp. G392-G398 ◽  
Author(s):  
Edward Parr ◽  
Maria J. Pozo ◽  
Burton Horowitz ◽  
Mark T. Nelson ◽  
Gary M. Mawe
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Action Potential ◽  
Resting Membrane Potential ◽  
Plateau Phase ◽  
Related Gene ◽  
K Channels ◽  
Contraction Coupling

The current study was undertaken to test the existence and possible role of ether-a-go-go-related gene 1 (ERG1) protein K+ channels in gallbladder smooth muscle (GBSM). Transcripts encoding ERG1 were detected in human, mouse, and guinea pig GBSM, and ERG1 immunoreactivity was observed in GBSM cells. In intracellular voltage recordings, addition of E-4031 (100 nM–1 μM) or cisapride (100 nM–2 μM) caused concentration-dependent excitation of guinea pig GBSM that was not affected by 500 nM TTX + 5 μM atropine, and E-4031 also depolarized the resting membrane potential. In muscle strip studies, E-4031 either induced phasic contractions or significantly increased the amplitude of phasic contractions in spontaneously active tissues ( P = 0.001). E-4031 also potentiated bethanechol-induced contractions. In conclusion, ERG1 channels are expressed in the GBSM, where they play a role in excitation-contraction coupling probably by contributing to repolarization of the plateau phase of the action potential and to the resting membrane potential.

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.

Atherogenic Activity caused by Excess Membrane Cholesterol in Arterial Smooth Muscle: Role of Calcium Channels

1993 ◽  
pp. 107-115 ◽  
Author(s):  
Thomas N. Tulenko ◽  
R. Preston Mason ◽  
Meng Chen ◽  
Hiromi Tasaki ◽  
Daniel Rock ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Calcium Channels ◽  
Membrane Cholesterol ◽  
Arterial Smooth Muscle

scholarly journals The non-obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine

2008 ◽  
Author(s):  
Igor Buchwalow ◽  
Sona Cacanyiova ◽  
Joachim Neumann ◽  
Vera Samoilova ◽  
Werner Boecker ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Arterial Smooth Muscle
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