α1-Adrenoceptors: function and phosphorylation

García‐Sáinz, J. Adolfo; Vázquez‐Prado, José; Medina, Luz del Carmen

doi:10.1016/s0014-2999(99)00896-1

Cited by 123 publications

(92 citation statements)

References 69 publications

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“…PE-treated cells also had increased levels of glutamic acid and other amino acids when compared to CONTR (Table 3). Based on current knowledge about adrenergic receptor activation (Wu et al 1992;García-Sáinz 2000;Piascik and Perez 2001), assumptions can be made that stimulation of cultured N1E-115 cells with PE induces energydependent cellular processes. It therefore seems plausible that the observed reduction in carbohydrates may be the result of increased utilisation to meet a higher energy demand.…”

Section: Immunocytochemistry Of N1e-115 Cells Confirms Protein Expresmentioning

confidence: 99%

The potential of metabolomic analysis techniques for the characterisation of α1-adrenergic receptors in cultured N1E-115 mouse neuroblastoma cells

et al. 2015

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Several studies of neuropathic pain have linked abnormal adrenergic signalling to the development and maintenance of pain, although the mechanisms underlying this are not yet fully understood. Metabolomic analysis is a technique that can be used to give a snapshot of biochemical status, and can aid in the identification of the mechanisms behind pathological changes identified in cells, tissues and biological fluids. This study aimed to use gas chromatographymass spectrometry-based metabolomic profiling in combination with reverse transcriptase-polymerase chain reaction and immunocytochemistry to identify functional a 1 -adrenergic receptors on cultured N1E-115 mouse neuroblastoma cells. The study was able to confirm the presence of mRNA for the a 1D subtype, as well as protein expression of the a 1 -adrenergic receptor. Furthermore, metabolomic data revealed changes to the metabolite profile of cells when exposed to adrenergic pharmacological intervention. Agonist treatment with phenylephrine hydrochloride (10 lM) resulted in altered levels of several metabolites including myo-inositol, glucose, fructose, alanine, leucine, phenylalanine, valine, and n-acetylglutamic acid. Many of the changes observed in N1E-115 cells by agonist treatment were modulated by additional antagonist treatment (prazosin hydrochloride, 100 lM). A number of these changes reflected what is known about the biochemistry of a 1 -adrenergic receptor activation. This preliminary study therefore demonstrates the potential of metabolomic profiling to confirm the presence of functional receptors on cultured cells.

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Section: Immunocytochemistry Of N1e-115 Cells Confirms Protein Expresmentioning

confidence: 99%

The potential of metabolomic analysis techniques for the characterisation of α1-adrenergic receptors in cultured N1E-115 mouse neuroblastoma cells

et al. 2015

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“…Overall, the 1 -adrenoceptors cause vasoconstriction, relaxation of gastrointestinal smooth muscle, salivary secretion, and hepatic glycogenolysis (Pocock andRichards, 2006, Rang et al, 2007). 1 -Adrenoceptors are mainly coupled to G q/11 -protein with consequent activation of phospholipase C. Phospholipase C promotes the hydrolysis of phosphatidylinositol bisphosphate producing inositol trisphosphate and diacylglycerol (Docherty, 1998, Zhong and Minneman, 1999, García-Sáinz et al, 2000, Guimarães and Moura, 2001, which act as second messengers. Inositol trisphosphate mediates intracellular Ca 2+ release from non mitochondrial pools and, consequently, the activation of other Ca 2+ and calmodulin sensitive pathways such as CaMKII, whilst diacylglycerol activates PKC (Guimarães andMoura, 2001, Westfall andWestfall, 2006).…”

Section: Alpha (α)-Adrenoceptorsmentioning

confidence: 99%

“…The continuous exposure to adrenergic agonists causes a progressive decrease in the capacity to respond to those agents by catecholamine-sensitive cells. This phenomenon, often termed refractoriness, or desensitization, is another "check point" in neuroendrocrine regulation (García-Sáinz et al, 2000, Hoffmann, 2004. Two major types of desensitization have been distinguished: homologous and heterologous.…”

Section: Location and Regulation Of Adrenoceptorsmentioning

confidence: 99%

“…In heterologous desensitization, a decreased responsiveness is observed to an agent or agents unrelated to the initial stimulus. Certainly, this classification is only operational and both types of desensitization may occur simultaneously in the cells (García-Sáinz et al, 2000). Even so, the mechanisms are equally complex and need further characterization.…”

Section: Location and Regulation Of Adrenoceptorsmentioning

confidence: 99%

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Adrenaline and Noradrenaline: Partners and Actors in the Same Play"

Costa¹,

Carvalho²,

Bastos³

et al. 2012

Neuroscience - Dealing With Frontiers

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“…3). However, the further development of this contraction cannot not be predicted with confidence since it would be modulated by the diffusion rate and neuronal uptake of NA along with the ongoing desensitization of α1 receptors (Chalothron et al, 2002;Ferguson, 2001;García-Sáinz et al, 2000;Kenakin, 1980;Schomig et al, 1991). The oscillatory contractions are the least investigated aspect of the NA-induced contractions to date.…”

Section: Role Of Cell-to-cell Coupling In Na-induced Contractionmentioning

confidence: 99%

Effect of heptanol on noradrenaline-induced contractions in rat vas deferens

Palani

Manchanda

2006

J. Smooth Muscle Res.

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We have studied the effects of 1-heptanol and nifedipine on noradrenaline (NA)-induced contractions in order to explore the role of gap junctions and their interactions with L-type Ca 2+ channel mediated [Ca 2+ ]o entry in the generation of NA-induced contractions in the rat vas deferens. Application of 20 μM NA to rat vas deferens resulted in contractions with three different components, an initial phasic component followed by a tonic component overlapped with an oscillatory component. Heptanol (0.01-2 mM) induced a concentration dependent reduction of the contractions. 2 mM heptanol reduced the phasic component by 32.9 ± 4.4% and the tonic component by 93.8 ± 1.9% of control, while the oscillatory component was completely abolished (n=7). Nifedipine (2 μM) reduced the phasic component by 34.5 ± 4.1% and the tonic component by 89.5 ± 3.8% of control and abolished the oscillatory component (n=6). In the presence of heptanol and nifedipine together, the phasic component was reduced by 61.3 ± 8.3% and the tonic component by 94.5 ± 1.0% of control. The oscillatory component was completely abolished (n=6). These results allow the conclusion that phasic contraction is mainly due to the direct action of NA, independent of gap junctions, while the tonic and oscillatory contractions may depend significantly on cell-to-cell communication. These in turn may depend critically on the availability of extracellularly derived Ca 2+ .

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α1-Adrenoceptors: function and phosphorylation

Cited by 123 publications

References 69 publications

The potential of metabolomic analysis techniques for the characterisation of α1-adrenergic receptors in cultured N1E-115 mouse neuroblastoma cells

The potential of metabolomic analysis techniques for the characterisation of α1-adrenergic receptors in cultured N1E-115 mouse neuroblastoma cells

Adrenaline and Noradrenaline: Partners and Actors in the Same Play"

Effect of heptanol on noradrenaline-induced contractions in rat vas deferens

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