Vascular effects of free radicals generated by electrical stimulation

1984 ◽  
Vol 247 (5) ◽  
pp. H709-H714 ◽  
Author(s):  
F. S. Lamb ◽  
R. C. Webb
Keyword(s):  
Electrical Stimulation ◽  
Free Radical ◽  
Experimental System ◽  
Electrical Field Stimulation ◽  
Oxygen Metabolism ◽  
Inhibitory Effect ◽  
Oxygen Free Radical ◽  
Vascular Effects ◽  
Electrical Field ◽  
Rat Tail

Electrical field stimulation (9 V, 1.0 ms, 4 Hz) of isolated segments of rat tail arteries and dog coronary arteries inhibits contractile responses to exogenous norepinephrine and elevated potassium concentration. This inhibitory effect of electrical stimulation is blocked by various agents that alter oxygen metabolism: superoxide dismutase, catalase, glutathione, ascorbate, and dimethyl sulfoxide. The observations suggest that the inhibitory effect is due to an action of oxygen free radical metabolites that are generated by the electrical stimulation of the oxygen-rich buffer. These free radical metabolites have two actions: 1) they oxidize drugs in the experimental system, and 2) they exert a direct inhibitory action on vascular smooth muscle.

Alteration of exogenous norepinephrine caused by electrical 'field' stimulation and its role in poststimulant relaxation

1977 ◽  
Vol 55 (5) ◽  
pp. 990-1000 ◽  
Author(s):  
D. George Wyse
Keyword(s):  
Electrical Stimulation ◽  
Initial Level ◽  
Electrical Field Stimulation ◽  
Pharmacological Action ◽  
Dependent Manner ◽  
Field Stimulation ◽  
Electrical Field ◽  
Rabbit Ear ◽  
High Concentrations ◽  
Rat Tail

Arterial strips from rat tail, rabbit ear, and dog mesentery, which are partially contracted by norepinephrine (NE), relax below the initial level of contraction in a frequency-dependent manner after cessation of transmural electrical stimulation. Antagonism of poststimulant relaxation by several pharmacologically unrelated agents suggests that the phenomenon is probably not due to release of a specific dilator neurotransmitter. Indeed, electrical stimulation of modified Krebs bicarbonate solution (contains EDTA) and NE in the absence of tissue abolishes the ability of the mixture to elicit a contraction when transferred to a second bath containing unstimulated tissue. Electrical stimulation does not measurably alter bath pH and temperature nor the ability of NE and 5-hydroxytryptamine to elicit contractions when they are added to the bath after stimulation has ended. Electrical stimulation (30-s train, 16 Hz, 0.5 A, rectilinear pulse width 0.5 ms) of modified Krebs bicarbonate solution and radiolabelled NE in the presence or absence of tissue results in alteration of a major portion of the labelled NE with appearance of several unidentified products. High concentrations of a known NE metabolite (3,4-dihydroxyphenylglycol) interfere with the ability of NE to maintain a contraction, and the possibility that NE breakdown products may interfere with NE's pharmacological action as an additional mechanism for a portion of poststimulant relaxation is not excluded. It is concluded that 'field' stimulation under the present conditions causes oxidation of NE in spite of the usual precaution of adding EDTA to the bath solution.

Pharmacologic responses of the mouse urinary bladder

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 192-197 ◽  
Author(s):  
A. Canda ◽  
Christopher Chapple ◽  
Russ Chess-Williams
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Detrusor Muscle ◽  
Field Stimulation ◽  
Muscarinic Agonists ◽  
Electrical Field ◽  
M3 Receptor

AbstractThe aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

Nonadrenergic inhibitory nerves attenuate neurally mediated contraction in cat bronchi

1990 ◽  
Vol 69 (5) ◽  
pp. 1594-1598 ◽  
Author(s):  
T. Aikawa ◽  
K. Sekizawa ◽  
S. Itabashi ◽  
H. Sasaki ◽  
T. Takishima
Keyword(s):  
Contractile Response ◽  
Stimulus Frequency ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Inhibitory Effects ◽  
Electrical Field ◽  
Calcitonin Gene ◽  
Contraction And Relaxation ◽  
Biphasic Responses

Effects of nonadrenergic and noncholinergic (NANC) inhibitory nerves on cholinergic neurotransmission were examined in isolated bronchial segments from cats in the presence of propranolol (10(-6) M) and indomethacin (10(-6) M) by use of electrical field stimulation (EFS) techniques. EFS caused contraction alone in tissues at the baseline tension and biphasic responses (contraction and relaxation) in tissues precontracted with 5-hydroxytryptamine. Contraction was abolished by atropine (10(-6) M), and relaxation was abolished by tetrodotoxin (10(-6) M). At the baseline tension, EFS at frequencies greater than 10 Hz inhibited the subsequent (4 min later) contraction induced by EFS at 1-5 Hz. EFS-induced inhibition was stimulus frequency dependent and reached maximum at 20 Hz. However, EFS at 20 Hz did not inhibit the subsequent contractile response to acetylcholine (10(-7) to 10(-3) M). Exogenously applied vasoactive intestinal peptide mimicked EFS-induced inhibitory effects, but substance P and calcitonin gene-related peptide did not. The inhibitory effect of EFS at 20 Hz was not altered by pyrilamine, cimetidine, naloxone, methysergide, phentolamine, BW755C, AF-DX 116, or removal of epithelium. These results imply that the NANC transmitter acts via presynaptic cholinergic receptors.

Delayed shortening and shrinkage of cochlear outer hair cells

1992 ◽  
Vol 263 (5) ◽  
pp. C1088-C1095 ◽  
Author(s):  
S. Ohnishi ◽  
M. Hara ◽  
M. Inoue ◽  
T. Yamashita ◽  
T. Kumazawa ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Hair Cells ◽  
Cytochalasin B ◽  
Electrical Field Stimulation ◽  
Outer Hair Cells ◽  
Disulfonic Acid ◽  
Free Medium ◽  
Electrical Field ◽  
Cl Channels ◽  
Stimulation Of

Slow shortening of cochlear outer hair cells has been speculated to modify cochlear sensitivity. Tetanic electrical field stimulation of isolated outer hair cells from guinea pigs shortened the cells for 2-3 min. Electrical stimulation reduced cell length and volume (-13.5 +/- 1.5 and -37.3 +/- 3.0% of initial values, respectively, n = 16) and decreased the intracellular Cl- concentration. Cytochalasin B (100 microM) inhibited electrical stimulation-induced shortening but not volume reduction. The following chemicals or manipulations inhibited the responses: 10 microM furosemide, 0.1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), 1 mM anthracene-9-carboxylic acid (AC9), 25 mM tetraethylammonium, 2.3 microM charybdotoxin (ChTX), 250 nM omega-conotoxin, and Ca(2+)-free medium. These findings suggest that both electrical stimulation-induced shortening and shrinkage of outer hair cells result not only from an actin-mediated contractile force, but also from Cl- efflux through furosemide-, DIDS-, and AC9-sensitive Cl- channels, and K+ efflux through ChTX-sensitive K+ channels.

Bronchomotor responses of isolated sheep airways to electrical field stimulation

1982 ◽  
Vol 53 (5) ◽  
pp. 1088-1093 ◽  
Author(s):  
J. R. Sheller ◽  
K. L. Brigham
Keyword(s):  
Electrical Stimulation ◽  
Response Curve ◽  
Electrical Field Stimulation ◽  
Isometric Tension ◽  
Field Stimulation ◽  
Frequency Response Curve ◽  
Inhibitory System ◽  
Electrical Field ◽  
The Right ◽  
Trachea And Bronchi

To determine the functional innervation of sheep airway smooth muscle, we measured the isometric tension developed by sheep tracheal segments, bronchial rings, and lung parenchymal strips in response to electrical field stimulation (ES) in tissue chambers. The contractions caused by ES were abolished in trachea and bronchi by atropine 10(-6) M or tetrodotoxin 1.6 X 10(-6) M. The small contractions evoked in lung parenchymal strips were not affected by tetrodotoxin. Electrical stimulation in the presence of atropine 10(-6) M and phentolamine 10(-6) M caused a frequency-dependent reduction in serotonin-induced tension in tracheal segments and bronchial rings. Electrical stimulation had little or no effect on the tension evoked in lung parenchymal strips by acetylcholine 10(-5) M or to histamine 10(-6) M. Propranolol 10(-6) M or guanethidine 10(-5) M caused a shift to the right in the frequency-response curve of trachea and bronchi. These findings suggest the presence of cholinergic excitatory and adrenergic inhibitory innervation in larger sheep airways. A concomitant nonadrenergic inhibitory system may be present. The terminal bronchioles present in lung parenchymal strips do not appear to have an effective bronchomotor innervation.

Electrically stimulated contraction accelerates protein synthesis rates in adult feline cardiocytes

1993 ◽  
Vol 265 (2) ◽  
pp. H666-H674 ◽  
Author(s):  
C. T. Ivester ◽  
R. L. Kent ◽  
H. Tagawa ◽  
H. Tsutsui ◽  
T. Imamura ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Electrical Stimulation ◽  
Total Protein ◽  
Actinomycin D ◽  
Electrical Field Stimulation ◽  
Cell Protein ◽  
Electrical Field ◽  
Butanedione Monoxime ◽  
H Protein ◽  
Stimulation Of

Cardiocytes were induced to contract via electrical field stimulation with an 8 V/cm electrical square-wave pulse of 5 ms at 0.125-2.0 Hz for up to 6 h. Protein synthesis rates were measured as rate of incorporation of [3H]-phenylalanine into total cell protein. Rates of protein synthesis were accelerated 43 +/- 4%, P < 0.001, by 4 h. The acceleration of total protein synthesis showed a frequency dependence between 0.125 and 0.5 Hz. In addition to accelerating rates of total protein synthesis, electrical stimulation of contraction accelerated fractional rates of synthesis of myosin heavy chain by 42 +/- 8%, P < 0.05. Protein synthesis rates were not accelerated upon electrical stimulation using subthreshold voltages. Addition of 100 ng/ml of actinomycin D had no effect on the ability of electrical stimulation of contraction to accelerate protein synthesis. To uncouple excitation-contraction coupling, 2,3-butanedione monoxime (BDM) was used to block actin-myosin cross-bridge interactions. BDM significantly decreased the ability of electrical stimulation to accelerate protein synthesis rates.

Release of superoxide-dependent relaxing factor(s) from endothelial cells

1989 ◽  
Vol 257 (5) ◽  
pp. H1340-H1346 ◽  
Author(s):  
K. W. Hong ◽  
B. Y. Rhim ◽  
W. S. Lee ◽  
B. R. Jeong ◽  
C. D. Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Experimental System ◽  
Electrical Field Stimulation ◽  
Calcium Deficiency ◽  
Buffer Solution ◽  
Electrical Field ◽  
Control Value ◽  
Relaxing Factor ◽  
Vascular Dilatation ◽  
Cytochrome C Reduction

In the present work, an experimental system was designed to study superoxide anion radical, implicated as the cause of vascular dilatation. To circumvent its direct effect, we employed a two-bath system. When the endothelial cells (EC) were exposed to electrical field stimulation (EFS) or to a hypoxanthine-xanthine oxidase system in bath A plus its physiological buffer solution suffused on a helical strip of cat basilar artery in bath B, the contraction to 5-hydroxytryptamine (5-HT) was depressed to approximately 40-50% of the control value. The reduction was not elicited on EFS in a state of calcium deficiency or in the absence of EC. The depression could be prevented by pretreatment with superoxide dismutase (SOD), but not with an effective dose of catalase, dimethyl sulfoxide (DMSO), mannitol, or indomethacin. The percent depression of contraction was paralleled by an increase in SOD-inhibitable cytochrome c reduction, which was not associated with cyclic guanosine 3',5'-monophosphate formation. These results suggest that superoxide-dependent relaxing factor is released from EC differently than the endothelium-derived relaxing factor mediated by acetylcholine.

Hydrogen peroxide-induced potentiation of contractile responses in isolated rat airways

1990 ◽  
Vol 258 (4) ◽  
pp. L232-L237 ◽  
Author(s):  
J. L. Szarek ◽  
N. L. Schmidt
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Airway Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Airway Hyperreactivity ◽  
Field Stimulation ◽  
Electrical Field ◽  
Contractile Responses ◽  
Isolated Rat

We hypothesized that metabolites of O2 may play a role in the development of airway hyperreactivity and undertook this study to examine the effects of one of these metabolites, hydrogen peroxide (H2O2), on electrical field stimulation-induced contractile responses of isolated rat intrapulmonary bronchi. Exposure to H2O2 (1 mM) elicited a transient contractile response with a peak response equivalent to 18.1 +/- 2.0% of the reference contraction obtained to electrical stimulation. The H2O2-induced contraction was attenuated by pretreatment of tissues with indomethacin and superoxide dismutase, but abolished by catalase and mianserin. Subsequent to H2O2 exposure, electrical field stimulation-induced contractile responses were potentiated (P less than 0.0001), whereas acetylcholine-induced contractions were not. The potentiating effects of H2O2 were inhibited by catalase and mianserin. Addition of 5-hydroxytryptamine (5-HT) to the bath similarly potentiated contractions to electrical stimulation (P less than 0.0001). Together, these results are consistent with a role for 5-HT in H2O2-induced contraction and the subsequent potentiation of airway smooth muscle contraction elicited by cholinergic nerve activation. Thus endogenous metabolites of O2 may be important in modulating airway smooth muscle tone.

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