Membrane Potential and Relaxation in Vascular Smooth Muscle

2015 ◽  
pp. 56-72 ◽  
Author(s):  
G. Siegel ◽  
R. Ehehalt ◽  
H. P. Koepchen
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle

scholarly journals TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential‐dependent coupling with PTEN

2019 ◽  
Vol 33 (9) ◽  
pp. 9785-9796 ◽  
Author(s):  
Takuro Numaga‐Tomita ◽  
Tsukasa Shimauchi ◽  
Sayaka Oda ◽  
Tomohiro Tanaka ◽  
Kazuhiro Nishiyama ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phenotypic Switching ◽  
Plasma Membrane Potential

A synthetic transmembrane segment derived from TRPV4 channel self-assembles into potassium-like channels to regulate vascular smooth muscle cell membrane potential

2014 ◽  
Vol 2 (24) ◽  
pp. 3809-3818 ◽  
Author(s):  
Zhiqiang Yu ◽  
Jie Li ◽  
Jinhang Zhu ◽  
Min Zhu ◽  
Feifei Jiang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Membrane Potential ◽  
Trpv4 Channel ◽  
Muscle Cell Membrane

A synthetic K+-like channel mediates K+outward flow to regulate vascular smooth muscle cell membrane potential, blood vessel tone and blood pressure.

Comparison of the electrical properties of arterial smooth muscle in normotensive rats and rats with deoxycorticosterone acetate-salt-induced hypertension: Possible involvement of (Na+-K+-Cl−) co-transport

1991 ◽  
Vol 81 (1) ◽  
pp. 73-78 ◽  
Author(s):  
J. P. L. Davis ◽  
A. R. Chipperfield ◽  
A. A. Harper
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Sprague Dawley ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Na Permeability ◽  
K Concentration ◽  
K Permeability

1. Hypertension was induced in male Sprague-Dawley rats by left unilateral nephrectomy and deoxycorticosterone acetate-salt administration. After 5 weeks, arterial systolic blood pressure was significantly elevated in these animals (191.5 ± 6.0 mmHg, mean ± sd, n = 17) compared with age-matched, unoperated control animals (134.0 ± 4.2 mmHg, n = 8, P < 0.001). 2. The membrane potential of femoral artery vascular smooth muscle measured in vitro was −55.1 ± 6.3 mV (mean ± sd, n = 154) for normotensive and −50.8 ± 5.7 mV (n = 82) for hypertensive animals. The difference in membrane potential was significant (P < 0.001). 3. The relationship between the log of the extracellular K+ concentration and membrane potential was nonlinear over the extracellular K+ concentration range 2.5–20 mmol/l, and showed a small positive shift with hypertension. 4. Tenfold reductions in the extracellular concentrations of Na+ or Cl− resulted in a membrane potential hyperpolarization in vascular smooth muscle from normotensive animals (4.9 ± 2.0 mV, n = 13 and 12.1 ± 1.3 mV, mean ± sd, n = 14, respectively). In vascular smooth muscle from hypertensive animals, the hyperpolarization in low-Na+ media was significantly increased to 12.2 ± 2.6 mV (mean ± sd, n = 5), but that in low-Cl− media was unaffected (2.7 ± 1.6 mV, n = 6). 5. The loop diuretic, bumetanide (10 μmol/l), hyperpolarized the membrane potential in vascular smooth muscle from both normotensive and hypertensive rats, but not in low-Na+ or low-Cl− media. This effect was significantly increased in hypertension, from 1.8 ± 0.7 mV (mean ± sd, n = 8) to 4.0 ± 1.0 mV (n = 5). 6. These results suggest that in these cells, K+ permeability ≫ Na+ permeability > Cl− permeabilty, and that the membrane potential is determined principally by the K+ permeability. In deoxycorticosterone acetate-salt hypertension, the membrane potential is depolarized, Na+ permeability is substantially increased, and there appears to be an increase in the activity of the (Na+-K+-Cl−) co-transporter.

Role of Ba2+-resistant K+ channels in endothelium-dependent hyperpolarization of rat small mesenteric arteries

2004 ◽  
Vol 82 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Joke Breyne ◽  
Bert J Vanheel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electrical Response ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Combined Application ◽  
Junctional Coupling ◽  
A Minor

In rat small mesenteric arteries, the influence of modulation of basal smooth muscle K+ efflux on the mechanism of endothelium-dependent hyperpolarization was investigated. The membrane potentials of the vascular smooth muscle cells were measured using conventional microelectrode techniques. Incubation of resting arteries with the gap junction uncoupler carbenoxolone (20 µM) decreased the endothelium-dependent hyperpolarization elicited by a submaximal concentration of acetylcholine (3 µM) to about 65% of the control. In the presence of Ba2+ (200 µM), which depolarized the membrane potential by 10 mV, the acetylcholine-induced membrane potential response was doubled in magnitude, reaching values not different from control. Moreover, the hyperpolarization was more resistant to carbenoxolone in these conditions. Finally, both in the absence and in the presence of carbenoxolone, the combined application of Ba2+ and ouabain (0.5 mM) did not abolish the acetylcholine response. These results suggest that gap junctional coupling plays a role in endothelium-dependent hyperpolarization of smooth muscle cells of resting rat small mesenteric arteries. Additionally, these findings show that the hyperpolarization does not rely on activation of inward rectifying K+ channels. Although a minor contribution of Na–K pumping cannot be excluded, the Ba2+ experiments show that the membrane electrical response is mediated by activation of a Ba2+-resistant K+ conductance.Key words: EDHF, carbenoxolone, potassium channels, vascular smooth muscle cell membrane potential, vasodilation.

scholarly journals Differential effects of superoxide and hydrogen peroxide on myogenic signaling, membrane potential, and contractions of mouse renal afferent arterioles

2016 ◽  
Vol 310 (11) ◽  
pp. F1197-F1205 ◽  
Author(s):  
Lingli Li ◽  
En Yin Lai ◽  
Anton Wellstein ◽  
William J. Welch ◽  
Christopher S. Wilcox
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Perfusion Pressure ◽  
Principal Component ◽  
Muscle Cells ◽  
Luminal Diameter ◽  
Afferent Arterioles

Myogenic contraction is the principal component of renal autoregulation that protects the kidney from hypertensive barotrauma. Contractions are initiated by a rise in perfusion pressure that signals a reduction in membrane potential ( Em) of vascular smooth muscle cells to activate voltage-operated Ca2+ channels. Since ROS have variable effects on myogenic tone, we investigated the hypothesis that superoxide (O2·−) and H2O2 differentially impact myogenic contractions. The myogenic contractions of mouse isolated and perfused single afferent arterioles were assessed from changes in luminal diameter with increasing perfusion pressure (40–80 mmHg). O2·−, H2O2, and Em were assessed by fluorescence microscopy during incubation with paraquat to increase O2·− or with H2O2. Paraquat enhanced O2·− generation and myogenic contractions (−42 ± 4% vs. −19 ± 4%, P < 0.005) that were blocked by SOD but not by catalase and signaled via PKC. In contrast, H2O2 inhibited the effects of paraquat and reduced myogenic contractions (−10 ± 1% vs. −19 ± 2%, P < 0.005) and signaled via PKG. O2·− activated Ca2+-activated Cl− channels that reduced Em, whereas H2O2 activated Ca2+-activated and voltage-gated K+ channels that increased Em. Blockade of voltage-operated Ca2+ channels prevented the enhanced myogenic contractions with paraquat without preventing the reduction in Em. Myogenic contractions were independent of the endothelium and largely independent of nitric oxide. We conclude that O2·− and H2O2 activate different signaling pathways in vascular smooth muscle cells linked to discreet membrane channels with opposite effects on Em and voltage-operated Ca2+ channels and therefore have opposite effects on myogenic contractions.

Inhibition of hypoxia-induced calcium responses in pulmonary arterial smooth muscle by acetazolamide is independent of carbonic anhydrase inhibition

2007 ◽  
Vol 292 (4) ◽  
pp. L1002-L1012 ◽  
Author(s):  
Larissa A. Shimoda ◽  
Trevor Luke ◽  
J. T. Sylvester ◽  
Hui-Wen Shih ◽  
Ahamindra Jain ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Carbonic Anhydrase ◽  
Vascular Smooth Muscle ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Fluorescent Microscopy ◽  
Arterial Smooth Muscle ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle

Hypoxic pulmonary vasoconstriction (HPV) occurs with ascent to high altitude and can contribute to development of high altitude pulmonary edema (HAPE). Vascular smooth muscle contains carbonic anhydrase (CA), and acetazolamide (AZ), a CA inhibitor, blunts HPV and might be useful in the prevention of HAPE. The mechanism by which AZ impairs HPV is uncertain. Originally developed as a diuretic, AZ also has direct effects on systemic vascular smooth muscle, including modulation of pH and membrane potential; however, the effect of AZ on pulmonary arterial smooth muscle cells (PASMCs) is unknown. Since HPV requires Ca2+ influx into PASMCs and can be modulated by pH, we hypothesized that AZ alters hypoxia-induced changes in PASMC intracellular pH (pHi) or Ca2+ concentration ([Ca2+]i). Using fluorescent microscopy, we tested the effect of AZ as well as two other potent CA inhibitors, benzolamide and ethoxzolamide, which exhibit low and high membrane permeability, respectively, on hypoxia-induced responses in PASMCs. Hypoxia caused a significant increase in [Ca2+]i but no change in pHi. All three CA inhibitors slightly decreased basal pHi, but only AZ caused a concentration-dependent decrease in the [Ca2+]i response to hypoxia. AZ had no effect on the KCl-induced increase in [Ca2+]i or membrane potential. N-methyl-AZ, a synthesized compound lacking the unsubstituted sulfonamide group required for CA inhibition, had no effect on pHi but inhibited hypoxia-induced Ca2+ responses. These results suggest that AZ attenuates HPV by selectively inhibiting hypoxia-induced Ca2+ responses via a mechanism independent of CA inhibition, changes in pHi, or membrane potential.

48-h Hypoxic exposure results in endothelium-dependent systemic vascular smooth muscle cell hyperpolarization

2002 ◽  
Vol 283 (1) ◽  
pp. R79-R85 ◽  
Author(s):  
Scott Earley ◽  
Jay S. Naik ◽  
Benjimen R. Walker
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Vessel Wall ◽  
Hypoxic Exposure ◽  
Resting Membrane Potential ◽  
Resistance Arteries ◽  
Adrenergic Agonist ◽  
Intracellular Ca ◽  
Oxide Synthase

Chronic hypoxia (CH) results in reduced sensitivity to vasoconstrictors in conscious rats that persists upon restoration of normoxia. We hypothesized that this effect is due to endothelium-dependent hyperpolarization of vascular smooth muscle (VSM) cells after CH. VSM cell resting membrane potential was determined for superior mesenteric artery strips isolated from CH rats (Pb = 380 Torr for 48 h) and normoxic controls. VSM cells from CH rats studied under normoxia were hyperpolarized compared with controls. Resting vessel wall intracellular Ca2+ concentration ([Ca2+]i) and pressure-induced vasoconstriction were reduced in vessels isolated from CH rats compared with controls. Vasoconstriction and increases in vessel wall [Ca2+]i in response to the α1-adrenergic agonist phenylephrine (PE) were also blunted in resistance arteries from CH rats. Removal of the endothelium normalized resting membrane potential, resting vessel wall [Ca2+]i, pressure-induced vasoconstrictor responses, and PE-induced constrictor and Ca2+ responses between groups. Whereas VSM cell hyperpolarization persisted in the presence of nitric oxide synthase inhibition, heme oxygenase inhibition restored VSM cell resting membrane potential in vessels from CH rats to control levels. We conclude that endothelial derived CO accounts for persistent VSM cell hyperpolarization and vasoconstrictor hyporeactivity after CH.

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