Electrical membrane events in response to α-adrenoceptor stimulation

1985 ◽  
Vol 68 (s10) ◽  
pp. 51s-53s ◽  
Author(s):  
G. Haeusler ◽  
J. E. De Peyer
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Main Pulmonary Artery ◽  
Muscle Cells ◽  
Tension Development ◽  
Α2 Adrenoceptors ◽  
St 587

1. Strips of rabbit main pulmonary artery (RMPA) were used to study the effects of several agonists on tension development and membrane potential of the vascular smooth muscle cells. 2. The following α-adrenoceptor agonists were employed: methoxamine and St 587 (α1-selective), B-HT 920 (α2-selective) and clonidine, which stimulates preferentially α2-adrenoceptors. By the use of the selective antagonists prazosin and yohimbine it was not possible to differentiate convincingly between α1- and α2-adrenoceptors in the RMPA. Methoxamine and B-HT 920 produced depolarization of similar magnitude of the membrane of the vascular smooth muscle cells. In spite of these results, which point to a uniform α-adrenoceptor in the RMPA, contractions to α1-and α2-agonists differed in some important aspects. 3. Contractions in response to α2-agonists were highly susceptible to the inhibitory effects of calcium withdrawal and calcium antagonists whereas contractions to α1-agonists were much less so. Reduction of the membrane potential of the vascular cells by K+ at 12 mmol/l had no effect on the concentration-contraction curve of methoxamine but shifted that of B-HT 920 to the left. Conversely hyperpolarization of the membrane of the vascular smooth muscle cells by strychnine totally suppressed contraction to B-HT 920 and caused only a rightward shift of the concentration-contraction curve of methoxamine and St 587. 4. Interaction of α1- and α2-agonists with an apparently uniform α-adrenoceptor induces in the RMPA contraction which seems to be triggered by different membrane processes.

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

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.

Parathyroid hypertensive factor inhibits voltage-gated K+ channels in vascular smooth muscle cells

1999 ◽  
Vol 77 (11) ◽  
pp. 860-865 ◽  
Author(s):  
Jun Ren ◽  
Lei Zhang ◽  
Christina G Benishin
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Time Dependent ◽  
Delayed Rectifier ◽  
K Channels ◽  
Parathyroid Hypertensive Factor

Parathyroid hypertensive factor (PHF) has been implicated in regulation of vascular smooth muscle tone and pathogenesis of several forms of hypertension. Earlier studies have suggested that PHF enhances the actions of other vasoconstrictors, while it has no in vitro vasoconstrictor property of its own. PHF was previously found to enhance the L-type Ca channel currents and intracellular Ca responses to depolarization in vascular smooth muscle cells (VSMCs). The present study examined whether PHF might act on K channels in the plasma membrane of VSMCs. Primary cultured VSMCs from rat tail artery were used. The whole-cell version of the patch-clamp technique was used under conditions in which there was no contribution of Ca-activated K channels to the outward current. Both purified and semipurified PHF inhibited the delayed rectifier type potassium current in a dose-dependent manner. The effect was time dependent and was first significantly different from the control current after 30 min. The inhibition of the delayed rectifier K channel was associated with a time-dependent decrease in the resting membrane potential. Therefore, PHF may alter VSMC cellular Ca responses by reducing the membrane potential to a level closer to the activation potential of Ca channels.Key words: parathyroid hypertensive factor, hypertension, potassium channels, vascular smooth muscle, membrane potential.

scholarly journals Pharmacological inhibition of TRPM4 hyperpolarizes vascular smooth muscle

2010 ◽  
Vol 299 (5) ◽  
pp. C1195-C1202 ◽  
Author(s):  
Albert L. Gonzales ◽  
Zarine I. Garcia ◽  
Gregory C. Amberg ◽  
Scott Earley
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Membrane Depolarization ◽  
Intraluminal Pressure ◽  
Voltage Dependent ◽  
Arterial Constriction

The contractile state of vascular smooth muscle cells is regulated by small changes in membrane potential that gate voltage-dependent calcium channels. The melastatin transient receptor potential (TRP) channel TRPM4 is a critical mediator of pressure-induced membrane depolarization and arterial constriction. A recent study shows that the tricyclic compound 9-phenanthrol inhibits TRPM4, but not the related channel TRPM5. The current study investigated the specificity of 9-phenanthrol and the effects of the compound on pressure-induced smooth muscle depolarization and arterial constriction. Patch-clamp electrophysiology revealed that 9-phenanthrol blocks native TRPM4 currents in freshly isolated smooth muscle cells in a concentration-dependent manner (IC50 = 10.6 μM). 9-Phenanthrol (30 μM) had no effect on maximum evoked currents in human embryonic kidney cells expressing recombinant TRPC3 or TRPC6 channels. Large-conductance Ca2+-activated K+, voltage-dependent K+, inwardly rectifying K+, and voltage-dependent Ca2+ channel activity in native cerebral artery myocytes was not altered by administration of 9-phenanthrol (30 μM). Using intracellular microelectrodes to record smooth muscle membrane potential in isolated cerebral arteries pressurized to 70 mmHg, we found that 9-phenanthrol (30 μM) reversibly hyperpolarized the membrane from ∼−40 mV to ∼−70 mV. In addition, we found that myogenic tone was reversibly abolished when vessels were exposed to 9-phenanthrol. These data demonstrate that 9-phenanthrol is useful for studying the functional significance of TRPM4 in vascular smooth muscle cells and that TRPM4 is an important regulator of smooth muscle cell membrane depolarization and arterial constriction in response to intraluminal pressure.

Sign in / Sign up

Export Citation Format

Share Document