Effects of ascorbic acid and EDTA on vascular concentration-response to catecholamines

Maxwell, L. C.; Herlihy, Jeremiah T.; Riedel, G. L.

doi:10.1016/0026-2862(83)90057-2

Cited by 25 publications

(21 citation statements)

References 9 publications

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“…Cylindrical segments of thoracic aortae (8mm in length) were obtained from male Wistar rats (Maxwell et al, 1983).…”

Section: Methodsmentioning

confidence: 99%

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂

Marriott

1989

British J Pharmacology

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1 Noradrenaline (NA; ED9Q) caused a contraction of the rat aorta which could be separated into two components, a rapid response mediated by release of intracellular Ca2+ and a more slowly developing contraction which relied principally upon Ca2 + influx. 2 Exposure to acute (30min) hypoxia has been previously shown to reduce the NA-induced contraction (by 28.0 + 2.7%, n = 168) which recovered completely upon re-oxygenation (recovery response). In the present study, prolonged exposure to hypoxia (70h) caused a more pronounced reduction (39.7 + 3.0%, n = 90) of the NA-induced contraction, but, re-oxygenation then produced incomplete recovery to 77.9 + 3.9% (n = 90) of the control response.3 Prolonged exposure to 95% 02 caused a 36.5 + 3.1% (n = 42) reduction of NA-induced contractions, whereas prolonged exposure to 21% 02 only caused a small (12.6 + 3.4%, n = 6) depression of these responses. 4 The component of the NA-induced contraction mediated by release of intracellular Ca2+ is 39.8 + 1.3% (n = 83) of the NA contraction in Ca-containing Krebs solution and was previously found to be unaffected by acute hypoxia. However, following prolonged exposure to either hypoxia or 21% 02, this component only reached 30.7 + 2.2% (n = 32) or 28.3 + 0.9% (n = 6) of the control response, respectively. Prolonged exposure to 95%°2 caused a more pronounced reduction of this component of contraction which then reached 19.1 + 2.1% (n = 12) of the control response. 5 Verapamil (10nM-10uM) produced similar concentration-dependent reductions of NA-induced contractions elicited during control conditions or acute hypoxia; under these conditions, 1 gIM verapamil caused a 34.1 + 6.9% (n = 6) and a 41.8 + 2.9% (n = 18) reduction of these responses respectively. However, recovery responses caused by re-oxygenation of tissues exposed to acute hypoxia were more sensitive to verapamil which, at a concentration of 1 pm, caused a 59.2 + 2.7% (n = 18) reduction of these responses. Verapamil (10 nM-10 MM) also caused similar pronounced concentration-dependent reductions of contractions elicited during prolonged exposure to normoxia or hyperoxia and of recovery responses obtained following re-oxygenation of tissues exposed to prolonged hypoxia; 1 JM verapamil caused a 62.5 + 1.1% (n = 6), 77.2 + 3.8% (n = 12) and a 68.0 + 4.3% (n = 12) reduction of these responses respectively. In contrast, contractions elicited during prolonged hypoxia were less sensitive to verapamil which at a concentration of 1 JM only caused a 16.2 + 2.2% (n 12) reduction of these responses. 6 The present study indicates that prolonged exposure of the rat aorta to either hypoxic or oxygenated conditions causes attenuation of NA-induced contraction. However, these effects are also accompanied by changes in tissue Ca2+ handling which differ under each condition and might account for the observed modifications in tissue sensitivity to the calcium-entry blocker verapamil.

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“…Cylindrical segments of thoracic aortae (8mm in length) were obtained from male Wistar rats (Maxwell et al, 1983).…”

Section: Methodsmentioning

confidence: 99%

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂

Marriott

1989

British J Pharmacology

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“…After 24 h, the medium was replaced by fresh medium containing 50 mg/ml ascorbic acid (Eastman Organic Chemicals, Rochester, NY, USA), to prevent catecholamine degradation, [41][42][43] in the absence or presence of a signalling pathway inhibitor. A control triplicate received only medium.…”

Section: Calcium Determination By Confocal Microscopymentioning

confidence: 99%

Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

Scarparo

Visconti

Castrucci

2006

Cell Biochem. Funct.

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The biological effects of catecholamines in mammalian pigment cells are poorly understood, but in poikilothermic vertebrates they regulate the translocation of pigment granules. We have previously demonstrated in SK-Mel 23-human melanoma cells the presence of low affinity alpha(1)-adrenoceptors, which mediate a decrease in cell proliferation and increase in tyrosinase activity, with no change of tyrosinase expression. In this report, we investigated the signalling pathways involved in these responses. Calcium mobilization in response to phenylephrine (PHE), an alpha(1)-adrenergic agonist, was investigated by confocal microscopy, and no change of fluorescence during the treatment was observed, suggesting that calcium is not involved in the signalling pathway activated by alpha(1)-adrenoceptors in SK-Mel 23 cells. cAMP levels, determined by enzyme-immunoassay, were significantly increased by PHE (10(-5)-10(-4)M), that could be blocked by the alpha(1)-adrenergic antagonist benoxathian (10(-5)-10(-4)M). Several biological assays were then performed with PHE, for 72 h, in the absence or presence of various signalling pathway inhibitors, in an attempt to determine the intracellular messengers involved in the responses of proliferation and tyrosinase activity. Our results suggest the participation of p38 and ERKs in PHE-induced decrease of proliferation, and possibly also of cAMP and protein kinase A. Regarding PHE-induced increase of tyrosinase activity, it is suggested that the following signalling components are involved: cAMP/PKA, PKC, PI3K, p38 and ERKs.

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“…Tissues were maintained at 37°C in Krebs solution of the following composition (mM): NaCl 118.40, KCl 4.75, CaCl2 2.50, MgSO4 1.18, KH2PO4 1.19, NaHCO3 25.00 and glucose 11.66. EDTA (10 gM) and ascorbic acid (50 ILM) were also included to reduce the degradation of noradrenaline (NA) (Maxwell et al, 1983). …”

Section: Preparationsmentioning

confidence: 99%

An investigation of the actions of diltiazem on rat aorta exposed to acute hypoxia followed by re‐oxygenation

Marriott

1987

British J Pharmacology

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Effects of ascorbic acid and EDTA on vascular concentration-response to catecholamines

Cited by 25 publications

References 9 publications

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂

Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

An investigation of the actions of diltiazem on rat aorta exposed to acute hypoxia followed by re‐oxygenation

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Effects of ascorbic acid and EDTA on vascular concentration-response to catecholamines

Cited by 25 publications

References 9 publications

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2

Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

An investigation of the actions of diltiazem on rat aorta exposed to acute hypoxia followed by re‐oxygenation

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The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂

The effects of verapamil upon noradrenaline‐induced contraction of the rat isolated aorta following acute and prolonged alterations in PO₂