Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Huynh, Tam T.; Hagen, Per Otto

doi:10.1006/jsre.1999.5600

Cited by 7 publications

(3 citation statements)

References 23 publications

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“…It is also suggested that coupling with a particular type of G-protein can be regulated by the location, phosphorylation and expression of GPCRs (Davies et al, 1999;Xiang et al, 2002;Hasseldine et al, 2003). The results presented in this study suggest that a1B-adrenoceptors can be coupled to both Gq-protein and Gi/oprotein in human osteoblasts.…”

Section: Discussionsupporting

confidence: 50%

Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Kodama

Togari

2013

British J Pharmacology

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BACKGROUND AND PURPOSERecent studies demonstrated that the sympathetic nervous system regulates bone metabolism via b2-adrenoceptors. Although a-adrenoceptors are also expressed in osteogenic cells, their functions in bone metabolism have been less studied. We previously demonstrated that noradrenaline suppressed potassium currents via a1B-adrenoceptors in the human osteoblast SaM-1 cell line. The aim of this study was to investigate the signal transduction pathway and the physiological role of noradrenaline in human osteoblasts in more detail. EXPERIMENTAL APPROACHTo investigate signal transduction through a1B-adrenoceptors, we used whole-cell patch clamp recording and Ca fluorescence imaging. Potassium channels regulate membrane potential and cell proliferation activity in non-excitable cells, so we evaluated cell proliferation activity by BrdU incorporation and WST assay. KEY RESULTSIn SaM-1 cells, bath-applied noradrenaline elevated intracellular Ca 2+ concentration and this effect was abolished by both chloroethylclonidine, an a1B-adrenoceptor antagonist, and U73122, a PLC inhibitor. However, the inhibitory effect of noradrenaline on whole-cell current was unaffected by U73122. In contrast, in cells pretreated with either Pertussis toxin, a Gi/o-protein-coupled receptor inhibitor, or gallein, a Gbg-protein inhibitor, the inhibitory effect of noradrenaline on whole-cell current was significantly suppressed. Noradrenaline-induced enhancement of cell proliferation was inhibited by CsCl, a non-selective potassium channel blocker, gallein and H89, a PKA inhibitor, but not by U73122. CONCLUSIONS AND IMPLICATIONSNoradrenaline facilitated cell proliferation by regulation of potassium currents in human osteoblasts via Gi/o-protein-coupled a1B-adrenoceptors, not via coupling to Gq-proteins. Abbreviationsa-MEM, a-modified minimum essential medium; BK channel, large-conductance calcium-activated potassium channel; BrdU, 5-bromo-2′

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Section: Discussionsupporting

confidence: 50%

Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Kodama

Togari

2013

British J Pharmacology

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“…, 1999; Piascik & Perez, 2001). The presence of functional α 1A ‐ and α 1B ‐adrenoceptors in the smooth muscle of EDV corresponds with the findings in other veins, such as the human saphenous vein ( α 1A and α 1B ), jugular vein ( α 1A ), human umbilical vein ( α 1B ) and ovine umbilical vein ( α 1A and α 1B ) (Hu & Dyer, 1997; Davies et al. , 1999; Errasti et al.…”

Section: Discussionsupporting

confidence: 85%

“…, 2003), rabbit (Satoh et al. , 1998; Davies et al. , 1999), dog (Argyle & McGrath, 2000), pig (Zhou et al.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological characterization ofα₁‐adrenoceptors in equine digital veins

Zerpa¹,

Bailey²,

Berhane³

et al. 2006

Vet Pharm & Therapeutics

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Alpha-adrenoceptors mediate contractile responses in equine digital veins (EDVs) and arteries. Vascular smooth muscle alpha(1)-adrenoceptor subtypes have been implicated in a number of conditions, such as acute equine laminitis, and are therapeutic targets for the treatment of this condition. Digital veins, rather than arteries, were investigated in the present study because they have been specifically implicated in the pathophysiology of acute laminitis. The order of potency of a series of alpha(1)-adrenoceptor-selective agonists and antagonists was determined in isolated rings of EDVs under conditions of isometric tension. A61603 was the most potent agonist, with a higher potency (76-fold greater) than phenylephrine (PHE), suggesting the presence of the alpha(1A)-adrenoceptor subtype. Prazosin (30 nm) caused competitive inhibition of the responses to A61603 and PHE, with pK(b) values of 8.05 +/- 0.28 and 8.20 +/- 0.27, respectively. In addition, the alpha(1A)-adrenoceptor antagonist, WB4101 (10 nm), also caused competitive inhibition of the responses to the two agonists, with pK(b) values of 8.37 +/- 0.16 and 8.54 +/- 0.23, respectively, confirming the presence of the alpha(1A)-adrenoceptor subtype in EDVs. The selective alpha(1D)-adrenoceptor antagonist, BMY7378 (100 nm) did not cause a significant change in the response to the agonists, giving lower pK(b) values (6.97 +/- 0.27 and 6.88 +/- 0.17 vs. A61603 and PHE, respectively). Chloroethylclonidine dihydrochloride (45 microm, 30 min), used to produce selective inactivation of alpha(1B)-adrenoceptors, caused noncompetitive inhibition of the response to PHE, but was without effect on the response to A61603. These findings indicate that EDVs possess at least two different alpha(1)-adrenoceptor populations, which are predominantly of the alpha(1A) and alpha(1B) subtypes. These data may assist in the development of more selective antagonists for therapeutic use in horses.

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Characterization of Dopamine-Mediated Relaxation in Experimental Vein Bypass Grafts

Huynh

Hagen

2000

Journal of Surgical Research

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Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Cited by 7 publications

References 23 publications

Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Pharmacological characterization ofα₁‐adrenoceptors in equine digital veins

Characterization of Dopamine-Mediated Relaxation in Experimental Vein Bypass Grafts

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Functional Characterization of α1-Adrenergic Receptors in Experimental Vein Grafts

Cited by 7 publications

References 23 publications

Noradrenaline stimulates cell proliferation by suppressing potassium channels via Gi/o‐protein‐coupled α1B‐adrenoceptors in human osteoblasts

Noradrenaline stimulates cell proliferation by suppressing potassium channels via Gi/o‐protein‐coupled α1B‐adrenoceptors in human osteoblasts

Pharmacological characterization ofα1‐adrenoceptors in equine digital veins

Characterization of Dopamine-Mediated Relaxation in Experimental Vein Bypass Grafts

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Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Noradrenaline stimulates cell proliferation by suppressing potassium channels via G_i/o‐protein‐coupled α_1B‐adrenoceptors in human osteoblasts

Pharmacological characterization ofα₁‐adrenoceptors in equine digital veins