Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KATP Channels Mediated

Ibogaine effects are mediated by cellular receptors, ATP depletion followed by ROS production and antioxidant enzyme activity elevation in a dose and time dependent manner. Since the role of KATP channels and β-adrenoceptors in ROS cellular circuit was established here we explored their role in ibogaine pro-antioxidant effectiveness. Single dose of ibogaine (10 mg/L i.e., 28.8 μmol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (β1 and β2 adrenoceptors selective antagonists) and glibenclamide (KATP sensitive channels inhibitor; only frequency) pre-treatment. In Ca2+-stimulated uteri, ibogaine decreased both amplitude and frequency after 4 h. Pre-treatment with propranolol abolished ibogaine induced amplitude lowering, while glibenclamide had no effect. In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased. Pre-treatment with both propranolol and glibenclamide abolished observed changes of antioxidant enzymes activity suggesting that ibogaine pro-antioxidative effectiveness is β-adrenergic receptors and KATP channels mediated.

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α-2 And β-adrenergic receptors mediate NE's biphasic effects on rat thick ascending limb chloride flux

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2001.281.3.r979 ◽

2001 ◽

Vol 281 (3) ◽

pp. R979-R986 ◽

Cited By ~ 14

Author(s):

Craig F. Plato

Keyword(s):

Adrenergic Receptors ◽

Receptor Activation ◽

Thick Ascending Limb ◽

Dependent Manner ◽

Sprague Dawley ◽

Chloride Flux ◽

Concentration Dependent Manner ◽

Β Adrenergic Receptors ◽

Isolated Rat

The sympathetic neurotransmitter norepinephrine (NE) influences renal sodium excretion via activation of adrenergic receptors. The thick ascending limb (THAL) possesses both α-2 and β-adrenergic receptors. However, the role(s) different adrenergic receptors play in how isolated THALs respond to NE are unclear. We tested the hypothesis that both α-2 and β-adrenergic receptors are responsive to NE in the isolated THAL, with α-2 receptors inhibiting and β-receptors stimulating chloride flux ( J Cl). THALs from male Sprague-Dawley rats were perfused in vitro, and the effects of 1) incremental NE, 2) the α-2 agonist clonidine, and 3) the β-agonist isoproterenol on J Cl were measured. Low concentrations (0.1 nM) of NE decreased J Clfrom a rate of 114.2 ± 8.1 to 93.5 ± 14.6 pmol · mm−1 · min−1( P < 0.05), with the nadir occurring at 1 nM (67.7 ± 8.8 pmol · mm−1 · min−1; P < 0.05). In contrast, greater concentrations of NE significantly increased J Cl from the nadir to a maximal rate of 131.0 ± 28.5 pmol · mm−1 · min−1 at 10 μM ( P < 0.05). To evaluate the adrenergic receptors mediating these responses, the THAL J Cl response to NE was measured in the presence of selective antagonists of β- and α-2 receptors. A concentration of NE (1 μM), which alone tended to increase J Cl, decreased THAL J Cl (from 148.9 ± 16.4 to 76.2 ± 13.6 pmol · mm−1 · min−1; P < 0.01) in the presence of the β-antagonist propranolol. In contrast, a concentration of NE (0.1 μM), which alone tended to decrease J Cl, increased THAL J Cl (from 85.5 ± 20.1 to 111.8 ± 20.1 pmol · mm−1 · min−1; P < 0.05) in the presence of the α-2 antagonist rauwolscine. To further clarify the role of different adrenergic receptors, selective adrenergic agonists were used. The α-2 agonist clonidine decreased J Cl from 102.4 ± 9.9 to 54.0 ± 15.7 pmol · mm−1 · min−1, a reduction of 49.1 ± 11.0% ( P < 0.02). In contrast, the β-agonist isoproterenol stimulated J Cl from 95.3 ± 11.6 to 144.1 ± 15.0 pmol · mm−1 · min−1, an increase of 56 ± 14% ( P < 0.01). We conclude that 1) the sympathetic neurotransmitter NE exerts concentration-dependent effects on J Cl in the isolated rat THAL, 2) selective α-2 receptor activation inhibits THAL J Cl, and 3) selective β-receptor activation stimulates THAL J Cl. These data indicate the response elicited by the isolated rat THAL to NE is dependent on the neurotransmitter concentration, such that application of NE in vitro biphasically modulates J Cl via differential activation of α-2 and β-adrenergic receptors in a concentration-dependent manner.

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STIMULATION OF β-ADRENERGIC RECEPTORS INHIBITS TUMOR NECROSIS FACTOR ALPHA RELEASE FROM THE ISOLATED RAT HEART

Critical Care Medicine ◽

10.1097/00003246-199912001-00168 ◽

1999 ◽

Vol 27 (Supplement) ◽

pp. A70

Author(s):

Walter H Newman ◽

Manuel R Castresana ◽

Zhongbiao Wang ◽

Martin L Dalton ◽

Debra J Warejcka

Keyword(s):

Tumor Necrosis Factor ◽

Adrenergic Receptors ◽

Tumor Necrosis ◽

Isolated Rat Heart ◽

Necrosis Factor Alpha ◽

Factor Alpha ◽

Β Adrenergic Receptors ◽

Necrosis Factor ◽

Isolated Rat ◽

Stimulation Of

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Characteristics of β-adrenergic receptors in longitudinal muscle membranes of rat uterus: Changes in kinetic properties of the receptor during gestation

Journal of Molecular Recognition ◽

10.1002/(sici)1099-1352(199605)9:3<233::aid-jmr264>3.0.co;2-# ◽

1996 ◽

Vol 9 (3) ◽

pp. 233-238 ◽

Cited By ~ 3

Author(s):

Yuji Kaneko ◽

Takuji Tsukamoto ◽

Tatsuhiko Kawarabayashi ◽

Masahiko Ikeda ◽

Hajime Sugimori

Keyword(s):

Adrenergic Receptors ◽

Longitudinal Muscle ◽

Kinetic Properties ◽

Rat Uterus ◽

Β Adrenergic Receptors

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Effects of verapamil on lipolysis due to dibutyryl cyclic AMP

Biochemical Journal ◽

10.1042/bj2200321 ◽

1984 ◽

Vol 220 (1) ◽

pp. 321-324 ◽

Cited By ~ 1

Author(s):

H Goko ◽

S Takashima ◽

S Shimizu ◽

S Kagawa ◽

A Matsuoka

Keyword(s):

Cyclic Amp ◽

Adrenergic Receptors ◽

Inhibitory Effect ◽

Dependent Manner ◽

Dibutyryl Cyclic Amp ◽

Alpha Adrenergic Receptors ◽

Biphasic Effect ◽

Adrenergic Antagonists ◽

Dose Dependent ◽

Isolated Rat

The effects of verapamil, a calcium antagonist, on lipolysis in isolated rat adipocytes were studied. Verapamil (100 microM) potentiated lipolysis due to dibutyryl cyclic AMP (Bt2cAMP) at submaximal concentrations, with or without extracellular Ca2+. Lipolysis due to 0.5 mM-Bt2cAMP was potentiated by verapamil in a dose-dependent manner up to 200 microM, whereas at concentrations higher than 100 microM the stimulatory effect of verapamil was progressively diminished with or without extracellular Ca2+. Verapamil showed only an inhibitory effect on lipolysis due to adrenaline (0.1-10 microM) or 3-isobutyl-1-methylxanthine (IBMX; 25-200 microM). The stimulatory effect of verapamil on lipolysis due to Bt2cAMP was not blocked by alpha-adrenergic antagonists. These results suggest (i) that verapamil has a biphasic effect on lipolysis due to Bt2cAMP and only an inhibitory effect on that due to adrenaline or IBMX, and (ii) that extracellular Ca2+ or alpha-adrenergic receptors are not involved in the action of verapamil.

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Trypsinization of bovine parathyroid cells abolishes Ca2+-regulated parathyroid hormone secretion

Journal of Endocrinology ◽

10.1677/joe.0.1220213 ◽

1989 ◽

Vol 122 (1) ◽

pp. 213-218 ◽

Cited By ~ 2

Author(s):

R. Muff ◽

J. A. Fischer

Keyword(s):

Protein Kinase C ◽

Parathyroid Hormone ◽

Protein Kinase ◽

Adrenergic Receptors ◽

Hormone Secretion ◽

Dependent Manner ◽

Kinase C ◽

And Control ◽

Β Adrenergic Receptors ◽

Dose Dependent

ABSTRACT The secretion of parathyroid hormone (PTH) is inversely related to the extracellular Ca2+ concentration (Cae2+). To test the hypothesis that a Ca2+ sensor on the surface of parathyroid cells is involved in Ca2+-regulated PTH secretion, limited trypsinization of bovine parathyroid cells was carried out. Treatment with trypsin (1·1–10 mg/ml) inhibited, in a dose-dependent manner, PTH secretion stimulated by lowering Cae2+ from 2·0 to 0·5 mmol/l. In control cells, activation of protein kinase C with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced PTH secretion at 2·0 mmol Cae2+/1 but not at 0·5 mmol Cae2+/1. In trypsinized cells, however, TPA enhanced PTH secretion at both 0·5 and 2·0 mmol Cae2+/1. Isoproterenol-stimulated PTH secretion was maintained in trypsinized cells, but reduced cyclic AMP production revealed that some β-adrenergic receptors were destroyed. The cytosolic free Ca2+ concentration (Cai2+), as measured with fura-2, was raised within seconds in response to increasing Cae2+ from 0·5 to 2·0 mmol/l and was then lowered within 1 min to a sustained plateau; the changes were the same in trypsinized and control cells. In conclusion, trypsinization of parathyroid cells abolished Ca2+-regulated PTH secretion without affecting Cai2+. Journal of Endocrinology (1989) 122, 213–218

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Effects of NaCl on growth, ion accumulation, protein, proline contents and antioxidant enzymes activity in callus cultures of Jatropha curcas

Biologia ◽

10.2478/s11756-008-0054-7 ◽

2008 ◽

Vol 63 (3) ◽

Cited By ~ 25

Author(s):

Nitish Kumar ◽

Sudheer Pamidimarri ◽

Meenakshi Kaur ◽

Girish Boricha ◽

Muppala Reddy

Keyword(s):

Antioxidant Enzymes ◽

Jatropha Curcas ◽

Nacl Stress ◽

Callus Cultures ◽

Ion Accumulation ◽

Cellular Damage ◽

Dependent Manner ◽

Economic Potential ◽

Concentration Dependent Manner ◽

Enzymes Activity

AbstractJatropha curcas is an oil bearing species with multiple uses and considerable economic potential as a biofuel crop. The effect of NaCl stress on growth, ion accumulation, contents of protein, proline, and antioxidant enzymes activity in callus cultures of J. curcas was investigated. Exposure of callus to NaCl decreased growth in a concentration dependent manner. NaCl treated callus accumulated Na and declined in K, Ca and Mg contents. Na/K ratio increased steadily as a function of external NaCl treatment. NaCl induced significant differences in quality and quantity of proteins, whereas, proline accumulation remained more or less constant with treatment. NaCl stress enhanced the activity of superoxide dismutase (SOD; E.C. 1.15.1.1) and peroxidase (POX; E.C. 1.11.1.7). Further in the isoenzyme studies, four SOD isoenzymes (SOD 1, 2, 3, and 4) and two POX isoenzymes (POX 1 and 2) were detected with the treatment. NaCl strongly induced activity of SOD 4 isoenzyme in 40, 60, 80 mM and POX 2 isoenzyme in 40 and 80 mM NaCl concentrations. Increase in antioxidant enzymes activity could be a response to cellular damage induced by NaCl. This increase could not stop the deleterious effects of NaCl, but it reduced stress severity and thus allowed cell growth to occur.

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MECHANISM OF OESTRADIOL ACTION ON THE RAT UTERUS: INDEPENDENCE OF CYCLIC AMP, PROSTAGLANDIN E2 AND β-ADRENERGIC MEDIATION

Journal of Endocrinology ◽

10.1677/joe.0.0580525 ◽

1973 ◽

Vol 58 (3) ◽

pp. 525-533 ◽

Cited By ~ 22

Author(s):

U. ZOR ◽

Y. KOCH ◽

S. A. LAMPRECHT ◽

J. AUSHER ◽

H. R. LINDNER

Keyword(s):

Cyclic Amp ◽

Adrenergic Receptors ◽

Tissue Concentration ◽

Ovariectomized Rats ◽

Minor Role ◽

Prostaglandin E ◽

Rat Uterus ◽

Stimulatory Action ◽

Β Adrenergic Receptors

SUMMARY The hypothesis that cyclic AMP plays an essential role in mediating the biological action of oestradiol on the uterus, was tested by determining the tissue concentration of the cyclic nucleotide after incubation of uteri of immature rats with oestradiol or after injection of this steroid into immature or ovariectomized rats. The effect of known stimulants of uterine adenyl cyclase, namely β-adrenergic drugs and prostaglandin E2 (PGE2), on the level of cyclic AMP in the uterus was also examined both in vitro and in vivo. In either system, oestradiol failed to enhance the concentration of cyclic AMP in the uterine tissue, whereas adrenaline or the almost purely β-adrenergic agonist isoprenaline (isoproterenol) caused cyclic AMP accumulation that was susceptible to inhibition by the β-adrenergic blocking agent propranolol. Prostaglandin E2, and to a much lesser degree prostaglandin F2α, increased cyclic AMP concentration in the uterus, but the effect of PGE2 was not inhibited by propranolol. It may be concluded that oestradiol does not cause appreciable stimulation of PGE2 synthesis or activation of β-adrenergic receptors in the rat uterus since, otherwise, increased cyclic AMP production should have been observed after the treatment with oestradiol. Isoprenaline mimicked the stimulatory action of oestradiol on uterine ornithine decarboxylase. However, this action of isoprenaline was abolished by propranolol, whereas that of oestradiol was only slightly, though significantly, inhibited. The present findings do not support the view that the action of oestradiol on the uterus is mediated by cyclic AMP, and also suggest that β-adrenergic receptors and PGE2 can have only a minor role, if any, in the mechanism of action of this hormone.

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