Tetrodotoxin-resistant relaxation to transmural nerve stimulation in canine saphenous veins: a possible neural origin

1986 ◽  
Vol 64 (10) ◽  
pp. 1328-1334 ◽  
Author(s):  
Manohara P. J. Senaratne ◽  
Tissa Kappagoda
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Nerve Stimulation ◽  
Contractile Response ◽  
Neural Mechanism ◽  
Canine Saphenous Vein ◽  
Saphenous Veins ◽  
Neural Origin ◽  
Prostaglandin F ◽  
Relaxation Maximum

Transmural nerve stimulation following sympathetic (guanethidine 10−4 mol/L, phenoxybenzamine 2 × 10−5 mol/L, propranolol 2 × 10−6 mol/L) and muscarinic blockade (atropine 5 × 10−5 mol/L) produces a relaxatory response in canine saphenous veins contracted with prostaglandin F2α. This relaxatory response was shown previously to be resistant to tetrodotoxin. Transmural nerve stimulation (10 V, 1.0 ms) was applied as intermittent trains of stimuli of 30 s duration at frequencies of 1–32 Hz. The veins showed a frequency dependent relaxation (maximum 2.65 ± 0.20 g). The stimulations were repeated in the presence of lignocaine (10−3 mol/L), apamin (10−8 mol/L), ascorbic acid (10−4 mol/L), or catalase (50 μg/mL). The relaxatory response was unaffected by apamin, scorpion toxin, superoxide dismutase, ascorbic acid, and catalase (p > 0.05). However, lignocaine (10−3 mol/L) reduced significantly the relaxatory response to transmural nerve stimulation in this preparation (p < 0.05). In a separate group of veins, lignocaine (10−3 mol/L)l abolished the contractile response to transmural nerve stimulation with little effect upon the contractile response to exogenous noradrenaline and the relaxatory responses to isoprenaline and sodium nitrite. These findings support the proposition that the nonadrenergic, noncholinergic tetrodotoxin-resistant relaxatory response observed with transmural nerve stimulation in the canine saphenous vein is mediated by a neural mechanism.

Tetrodotoxin-resistant relaxation to transmural nerve stimulation in isolated saphenous vein

1984 ◽  
Vol 247 (6) ◽  
pp. H952-H959
Author(s):  
M. Senaratne ◽  
T. Kappagoda
Keyword(s):  
Smooth Muscle ◽  
Direct Effect ◽  
Nerve Stimulation ◽  
Saphenous Vein ◽  
Krebs Solution ◽  
Atpase Inhibitor ◽  
Frequency Dependent ◽  
Prostaglandin F2 Alpha ◽  
Saphenous Veins ◽  
Relaxation Maximum

The response to transmural nerve stimulation (TNS) was characterized in rings of canine saphenous veins following sympathetic (guanethidine 10(-4) mol/l; phenoxybenzamine 2 X 10(-5) mol/l; propranolol 2 X 10(-6) mol/l) and muscarinic blockade (atropine 5 X 10(-6) mol/l). In preparations which were contracted with prostaglandin F2 alpha, TNS was applied as intermittent trains of stimuli of 30 s duration at frequencies of 1-32 Hz. This stimulus elicited a frequency-dependent relaxation [maximum relaxation 3.4 +/- 0.21 (SE) g]. This relaxation was present in rings denuded of endothelium and was not altered significantly by cimetidine (10(-4) mol/l), indomethacin (10(-5) mol/l), aminophylline (10(-5) mol/l),or cyproheptadine (10(-6) mol/l). It was abolished by the Na+-K+-ATPase inhibitor ouabain (2 X 10(-4) mol/l) and in zero-K+ Krebs solution. When the experiment was repeated following storage of the isolated saphenous veins for 9 days at 4 degrees C TNS failed to induce any relaxation. However, the relaxation in fresh rings was not abolished by tetrodotoxin (10(-6) mol/l). The present study demonstrates a nonadrenergic noncholinergic relaxation to TNS in the saphenous vein which could be mediated by 1) a tetrodotoxin-resistant nerve or 2) a direct effect of TNS on the smooth muscle.

Hyperosmolarity: effects on nerves and smooth muscle of cutaneous veins

1976 ◽  
Vol 231 (1) ◽  
pp. 141-147 ◽  
Author(s):  
MA McGrath ◽  
JT Shepherd
Keyword(s):  
Smooth Muscle ◽  
Nerve Stimulation ◽  
Contractile Response ◽  
Total Radioactivity ◽  
Ringer Solution ◽  
Isometric Tension ◽  
Organ Bath ◽  
Free Medium ◽  
Saphenous Veins ◽  
Slow Contraction

Helical strips from dogs' saphenous veins were mounted in an organ bath (Krebs-Ringer solution, 37 degrees C) for isometric tension recording. Additional strips were incubated with [7-3H]norepinephrine and mounted for superfusion and isometric tension recording. The perfusate was collected every 2 min for estimation of total radioactivity and for column chromatographic separation of [3H]norepinephrine and its metabolites. Increasing osmolarity by sucrose caused a slow contraction that was maximal at 500-550 mosM and was accompanied by a reduction in total 3H efflux. The contraction was unaffected by a Ca2+-free medium, alpha-adrenegic blockade, and beta-adrenergic stimulaton. It was depressed by cooling (29 degrees C) and by anoxia combined with a glucose-free medium. Contractions elicited by K+ and Ba2+ were augmented by hyperosmolarity, but those caused by sympathetic nerve stimulation, tyramine, and norepinephrine were depressed. The output of [3H]norepinephrine during nerve stimulation was reduced. Thus, the hyperosmolarity causes 1) contraction of vascular smooth muscle, 2) augmentation of the contractile response to K+ and Ba2+, 3) depression of the excitation caused by norepinephrine, and 4) inhibition of the neuronal release of norepinephrine.

Ascorbic acid and CoQ10 ameliorate the reproductive ability of superoxide dismutase 1-deficient female mice†

2019 ◽  
Author(s):  
Naoki Ishii ◽  
Takujiro Homma ◽  
Jaeyong Lee ◽  
Hikaru Mitsuhashi ◽  
Ken-ichi Yamada ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Coenzyme Q10 ◽  
Knockout Mice ◽  
Knockout Mouse ◽  
Superoxide Dismutase 1 ◽  
Wild Type ◽  
Positive Effects ◽  
Reproductive Ability ◽  
Ascorbic Acid Supplementation

Abstract Superoxide dismutase 1 suppresses oxidative stress within cells by decreasing the levels of superoxide anions. A dysfunction of the ovary and/or an aberrant production of sex hormones are suspected causes for infertility in superoxide dismutase 1-knockout mice. We report on attempts to rescue the infertility in female knockout mice by providing two antioxidants, ascorbic acid and/or coenzyme Q10, as supplements in the drinking water of the knockout mice after weaning and on an investigation of their reproductive ability. On the first parturition, 80% of the untreated knockout mice produced smaller litter sizes compared with wild-type mice (average 2.8 vs 7.3 pups/mouse), and supplementing with these antioxidants failed to improve these litter sizes. However, in the second parturition of the knockout mice, the parturition rate was increased from 18% to 44–75% as the result of the administration of antioxidants. While plasma levels of progesterone at 7.5 days of pregnancy were essentially the same between the wild-type and knockout mice and were not changed by the supplementation of these antioxidants, sizes of corpus luteum cells, which were smaller in the knockout mouse ovaries after the first parturition, were significantly ameliorated in the knockout mouse with the administration of the antioxidants. Moreover, the impaired vasculogenesis in uterus/placenta was also improved by ascorbic acid supplementation. We thus conclude that ascorbic acid and/or coenzyme Q10 are involved in maintaining ovarian and uterus/placenta homeostasis against insults that are augmented during pregnancy and that their use might have positive effects in terms of improving female fertility.

Changes of superoxide dismutase activity and ascorbic acid in focal cerebral ischaemia in rats

1992 ◽  
Vol 14 (1) ◽  
pp. 26-30 ◽  
Author(s):  
Kiyoshi Takagi ◽  
Hideaki Kanemitsu ◽  
Noriko Tomukai ◽  
Hidemune Oka ◽  
Akira Tamura ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Cerebral Ischaemia ◽  
Superoxide Dismutase Activity ◽  
Focal Cerebral Ischaemia

Adrenergic control of intrarenal arteries of rabbits

1989 ◽  
Vol 256 (3) ◽  
pp. H607-H612
Author(s):  
M. P. Owen ◽  
M. C. Taphorn ◽  
J. G. Walmsley
Keyword(s):  
Smooth Muscle ◽  
Comparative Study ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Nerve Stimulation ◽  
Contractile Response ◽  
Vessel Diameter ◽  
Cell Stress ◽  
Adrenergic Control ◽  
Evoked Contractions

A comparative study of the adrenergic control of two sequential rabbit intrarenal arteries of differing diameter [intrarenal branch artery (IRBA)-unstretched lumen diameter (ULD) approximately 300 microns and interlobar artery (ILA)-ULD approximately 250 microns] has been conducted. The neurogenic contractile response of isolated segments in relation to the maximum response to l-norepinephrine (NE) was minimal (8 Hz response approximately 30% of maximum contraction) and similar in both types of arteries. Phentolamine (PTA) (10(-6) M) blocked neurally evoked contractions of the IRBAs at 2, 4, and 8 Hz and of the ILAs at 2 and 4 Hz. (8 Hz responses were not entirely blocked in 3 out of 8 ILAs.) The sensitivity to exogenous NE decreased with a decrease in intrarenal vessel diameter, whereas the maximum active smooth muscle cell stress to NE was greater than 3 X 10(5) N/m2 for each vessel. All arterial segments constricted in response to histamine (H) and NE with equal maximal effects; however, sensitivity to H was greater in the smaller artery (ILA). The comparative contractile responses to nerve stimulation and exogenous NE in sequential renal arteries contrasts to the pattern of these responses in sequential arteries in any other rabbit regional bed previously studied (pulmonary and ear vasculature).

scholarly journals Retinoic acid modulation of glutathione and cysteine metabolism in chondrocytes

1996 ◽  
Vol 314 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Cristina C. TEIXEIRA ◽  
Irving M. SHAPIRO ◽  
Masashi HATORI ◽  
Ramesh RAJPUROHIT ◽  
Cameron KOCH
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Retinoic Acid ◽  
Critical Role ◽  
Phosphate Concentration ◽  
Antioxidant Systems ◽  
Chondrocyte Maturation ◽  
Medium Components ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

The major objective of this investigation was to determine the thiol status of chondrocytes and to relate changes in the level of glutathione and cysteine to maturation of the cells as they undergo terminal differentiation. Chondrocytes were isolated from the cephalic portion of chick embryo sterna and treated with all-trans retinoic acid for one week. We found that the addition of 100 nM retinoic acid to the cultures decreased the intracellular levels of glutathione and cysteine from 6.1 to 1.6 and 0.07 to 0.01 nmol/μg DNA respectively; retinoic acid also caused a decrease in the extracellular concentration of cysteine. The decrease in chondrocyte thiols was dose and time dependent. To characterize other antioxidant systems of the sternal cell culture, the activities of catalase, glutathione reductase and superoxide dismutase were determined. Activities of all of those enzymes were high in the retinoic acid-treated cells; the conditioned medium also contained these enzymes and the cytosolic isoenzyme of superoxide dismutase. We probed the specificity of the thiol response by using immature caudal chondrocytes. Unlike the cephalic cells, retinoic acid did not change intracellular glutathione and extracellular cysteine levels, although the retinoid caused a reduction in the intracellular cysteine concentration. Finally, we explored the effect of medium components on chondrocyte thiol status. We noted that while ascorbate alone did not change cell thiol levels, it did cause a 4-fold decrease in the extracellular cysteine concentration. When retinoic acid and ascorbic acid were both present in the medium, there was a marked decrease in the level of glutathione. In contrast, the phosphate concentration of the culture medium served as a powerful modulator of both glutathione and cysteine. Results of the study clearly showed that there is a profound decrease in intracellular levels of both cysteine and glutathione and that thiol levels are responsive to ascorbic acid and the medium phosphate concentration. These findings point to a critical role for thiols in modulating events linked to chondrocyte maturation and cartilage matrix synthesis and mineralization.

Contractile response of fescue-naïve bovine lateral saphenous veins to increasing concentrations of tall fescue alkaloids1,2

2010 ◽  
Vol 88 (1) ◽  
pp. 408-415 ◽  
Author(s):  
J. L. Klotz ◽  
B. H. Kirch ◽  
G. E. Aiken ◽  
L. P. Bush ◽  
J. R. Strickland
Keyword(s):  
Tall Fescue ◽  
Contractile Response ◽  
Saphenous Veins

Norepinephrine-stimulated vascular prostacyclin synthesis. Receptor-dependent calcium channels control prostaglandin synthesis

1984 ◽  
Vol 62 (12) ◽  
pp. 1341-1347 ◽  
Author(s):  
Duncan Stewart ◽  
Elaine Pountney ◽  
David Fitchett
Keyword(s):  
Contractile Response ◽  
Fold Increase ◽  
Maximal Stimulation ◽  
Norepinephrine Concentration ◽  
Adrenergic Antagonist ◽  
Channel Blocking ◽  
Intracellular Ca ◽  
Prostaglandin F ◽  
Wet Weight ◽  
Prostacyclin Synthesis

Norepinephrine-stimulated prostacyclin synthesis was studied in rat aortic rings by measuring 6-keto-prostaglandin F1α (6-keto-PGF1α) by radioimmunoassay. Norepinephrine (10−6 M) results in a 10- to 20-fold increase in 6-keto-PGF1α synthesis by rat aortic rings (54 ± 11 to 437 ± 260 pg∙mg wet weight−1∙20 min−1). The maximal stimulation of 6-keto-PGF1α synthesis was observed with a norepinephrine concentration of 10−5 M at a mean effective concentration (EC50) of 9.5 ± 3.2 × 10−7 M which is similar to the contractile response (Emax = 10−5 M, EC50 = 6.5 ± 1.8 × 10−7 M). Potassium chloride (30 mM), although causing a similar maximal contractile response as 10−6 M norepinephrine, did not increase 6-keto-PGF1α synthesis. Norepinephrine-stimulated 6-keto-PGF1α synthesis was dependent upon extracellular calcium. Norepinephrine stimulation in Ca2+-free medium did not lead to a significant increase in 6-keto-PGF1α synthesis. However, on the introduction of Ca2+, 6-keto-PGF1α synthesis was restored to its initial level. Phentolamine (10−6 M) (an α-adrenergic antagonist) and trifluroperazine (2.5 × 10−4 M) (a calmodulin inhibitor) completely inhibited norepinephrine-stimulated 6-keto-PGF1α synthesis, whereas verapamil 3 × 10−6 M (a calcium channel blocking drug) only partially inhibited synthesis (control, 74 ± 12; norepinephrine, 437 ± 260; norepinephrine + verapamil, 123 ± 8 pg∙mg wet weight−1∙20 min−1). Norepinephrine-stimulated prostacyclin synthesis is probably α-receptor mediated and appears to depend upon the opening of receptor-operated Ca2+ channels. The operation of potential-dependent Ca2+ channels (by 30 mM KCl) in contrast, although known to be associated with an increase of intracellular Ca2+, does not stimulate PG synthesis.

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