scholarly journals Epoxyeicosatrienoic acids act through TRPV4–TRPC1–KCa1.1 complex to induce smooth muscle membrane hyperpolarization and relaxation in human internal mammary arteries

2015 ◽  
Vol 1852 (3) ◽  
pp. 552-559 ◽  
Author(s):  
Yan Ma ◽  
Peng Zhang ◽  
Jie Li ◽  
Jun Lu ◽  
Jianjun Ge ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Membrane ◽  
Epoxyeicosatrienoic Acids ◽  
Membrane Hyperpolarization ◽  
Mammary Arteries ◽  
Internal Mammary ◽  
Smooth Muscle Membrane

Endothelium-dependent hyperpolarization elicited by adenine compounds in rabbit carotid artery

1991 ◽  
Vol 260 (4) ◽  
pp. H1037-H1042 ◽  
Author(s):  
G. Chen ◽  
H. Suzuki
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Direct Action ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Dependent Manner ◽  
Rabbit Carotid Artery ◽  
Mechanical Removal ◽  
Smooth Muscle Membrane ◽  
Adventitial Cells

Electrical responses of the membrane of intimal and adventitial smooth muscle cells of the rabbit carotid artery to ATP, ADP, AMP, and adenosine were recorded. In intimal cells, these compounds hyperpolarized the membrane. Mechanical removal of the endothelium altered the responses to ATP and ADP to one of a transient depolarization, with no alteration of the response to AMP and adenosine. In the adventitial cells, ATP and ADP produced a transient depolarization, whereas AMP and adenosine produced a sustained hyperpolarization, irrespective of the presence or absence of the endothelium. In tissues with an intact endothelium, 5'-adenylylimidodiphosphate tetralithium salt and alpha,beta-methylene ATP (mATP) transiently depolarized the membrane in these smooth muscles. In case of stabilization with mATP, only hyperpolarization was generated by ATP, in an endothelium-dependent manner. Our interpretation of these observations is that 1) ATP and ADP depolarize smooth muscle membrane by a direct action and hyperpolarize the membrane indirectly through the release of endothelium-derived hyperpolarizing factor, 2) AMP and adenosine hyperpolarize the membrane, independently of the endothelium, and 3) ATP receptors present on the endothelial cell membrane differ from those on smooth muscle membrane.

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

Neuromuscular mechanisms of esophageal responses at and proximal to a distending balloon

1991 ◽  
Vol 260 (1) ◽  
pp. G148-G155 ◽  
Author(s):  
W. G. Paterson
Keyword(s):  
Smooth Muscle ◽  
Pressure Fluctuations ◽  
Muscle Membrane ◽  
Cholinergic Transmission ◽  
Spike Burst ◽  
Smooth Muscle Membrane ◽  
Cervical Vagotomy ◽  
Suction Electrode ◽  
Muscarinic Cholinergic ◽  
Alpha Chloralose

To determine the neuromuscular mechanisms involved in esophageal responses at and proximal to a distending stimulus, a manometric catheter incorporating a latex balloon at its distal end was positioned in the smooth muscle esophagus of alpha-chloralose-anesthetized opossums and used to record intraluminal pressures over the balloon and at several sites proximal to the balloon. Air inflation of the balloon evoked simultaneous phasic contractions at several sites proximal to the balloon that were abolished by bilateral cervical vagotomy. With the balloon located in the midesophagus, these proximal contractions were also abolished by atropine, and simultaneous suction electrode recordings indicated that they were associated with smooth muscle membrane depolarization and spike burst without preceding hyperpolarization. With the balloon located in the distal esophagus, the evoked proximal contractions were less atropine sensitive. Phasic pressure fluctuations recorded by the balloon itself were not affected by atropine or bilateral cervical vagotomy but were increased in amplitude by tetrodotoxin. These opossum studies suggest that unlike responses below a distending balloon, which have been shown to be noncholinergic and mediated by intramural neuromuscular mechanisms, proximal contractions depend on vagal pathways and, depending on esophageal location, muscarinic-cholinergic transmission. Contractions at the level of the distending balloon appear to be myogenic in origin.

11,12,15-Trihydroxyeicosatrienoic acid mediates ACh-induced relaxations in rabbit aorta

2003 ◽  
Vol 285 (6) ◽  
pp. H2648-H2656 ◽  
Author(s):  
William B. Campbell ◽  
Nancy Spitzbarth ◽  
Kathryn M. Gauthier ◽  
Sandra L. Pfister
Keyword(s):  
Smooth Muscle ◽  
Rabbit Aorta ◽  
Nordihydroguaiaretic Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
Muscle Membrane ◽  
Lipoxygenase Pathway ◽  
Lipoxygenase Inhibitors ◽  
Aortic Smooth Muscle ◽  
Threefold Increase ◽  
Smooth Muscle Membrane

Rabbit aortic endothelium metabolizes arachidonic acid (AA) by the 15-lipoxygenase pathway to vasodilatory eicosanoids, hydroxyepoxyeicosatrienoic acids (HEETAs), and trihydroxyeicosatrienoic acids (THETAs). The present study determined the chemical identity of the vasoactive THETA and investigated its role in ACh-induced relaxation in the rabbit aorta. AA caused endothelium-dependent, concentration-related relaxations of the rabbit aorta. Increasing the extracellular KCl concentration from 4.8 to 20 mM inhibited the relaxations to AA by ∼60%, thereby implicating K+-channel activation in the relaxations. In addition, AA caused an endothelium-dependent hyperpolarization of aortic smooth muscle from –39.6 ± 2.7 to –56.1 ± 3.4 mV. In rabbit aortic rings, [14C]AA was metabolized to prostaglandins, HEETAs, THETAs, and 15-hydroxyeicosatetraenoic acid. Additional purification of the THETAs by HPLC resolved the mixture into its 14C-labeled products. Gas chromatography/mass spectrometry identified the metabolites as isomers of 11,12,15-THETA and 11,14,15-THETA. The 11,12,15-THETA relaxed and hyperpolarized the rabbit aorta, whereas 11,14,15-THETA had no vasoactive effect. The relaxations to 11,12,15-THETA were blocked by 20 mM KCl. In aortic rings pretreated with inhibitors of nitric oxide and prostaglandin synthesis, ACh caused a concentration-related relaxation that was completely blocked by 20 mM KCl. Pretreatment with the phospholipase A2 inhibitors mepacrine and 7,7-dimethyl-5,8-eicosadienoic acid, the lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-α-cyanocinnamate, nordihydroguaiaretic acid, and ebselen, or the hydroperoxide isomerase inhibitors miconazole and clotrimazole also blocked ACh-induced relaxations. ACh caused a threefold increase in THETA release. These studies indicate that AA is metabolized by endothelial cells to 11,12,15-THETA, which activates K+ channels to hyperpolarize the aortic smooth muscle membrane and induce relaxation. Additionally, this lipoxygenase pathway mediates the nonnitric oxide, nonprostaglandin relaxations to ACh in the rabbit aorta by acting as a source of an endothelium-derived hyperpolarizing factor.

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