Abstract:
:The purpose of this study was to determine whether a cyclic adenosine 3',5'-monophosphate-dependent process can be involved in the regulation of vascular smooth muscle alpha 1-adrenergic receptor responsiveness. Experiments were performed in cultured rabbit aortic smooth muscle cells which were characterized previously according to alpha-adrenergic receptor-binding characteristics and receptor-coupled norepinephrine-stimulated 45Ca++ efflux. The addition of dibutyryl-cyclic adenosine monophosphate to the cell culture medium for 24 hours resulted in a concentration-related decrease in maximal [3H]prazosin-binding capacity (41 +/- 4% decrease with 1 mM dibutyryl-cyclic adenosine monophosphate) without an effect on [3H]prazosin-binding affinity. Prostaglandin E1 (10 microM) and forskolin (10 microM) caused similar decreases in maximal [3H]prazosin-binding capacity, whereas butyrate (1 mM) and dibutyryl-guanosine-3',5' cyclic-monophosphate (1 mM) had no effect. Dibutyryl-cyclic adenosine monophosphate (1 mM) caused significant potentiation of the decrease in [3H]prazosin-binding caused by a submaximal (10 nM) but not a maximal (10 microM) concentration of norepinephrine, suggesting that cyclic adenosine monophosphate may act at a distal step in common with norepinephrine to reduce alpha-adrenergic receptor number. Despite the approximately 41% reduction in alpha-adrenergic receptor number following 24-hour incubation of cells with dibutyryl-cyclic adenosine monophosphate, maximal norepinephrine-stimulated 45Ca++ efflux was not reduced, consistent with the markedly nonlinear relationship between alpha-adrenergic receptor occupancy and maximal norepinephrine-stimulated 45Ca++ efflux in this cell system. These data provide evidence for a novel mechanism by which hormones or drugs which increase cyclic adenosine monophosphate levels can modulate alpha-adrenergic responsiveness in vascular smooth muscle.
journal_name
Circ Resjournal_title
Circulation researchauthors
Colucci WSdoi
10.1161/01.res.58.2.292subject
Has Abstractpub_date
1986-02-01 00:00:00pages
292-7issue
2eissn
0009-7330issn
1524-4571journal_volume
58pub_type
杂志文章abstract::The present study investigated the effect of adrenomedullin, a novel vasorelaxant peptide, on the migration of cultured rat vascular smooth muscle cells (SMCs) by using the Boyden-chamber method. Fetal calf serum (FCS) and platelet-derived growth factor (PDGF)-BB strongly stimulated SMC migration. Adrenomedullin clear...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.77.4.660
更新日期:1995-10-01 00:00:00
abstract::During cardiac development, the epicardium is the source of multipotent mesenchymal cells, which give rise to endothelial and smooth muscle cells in coronary vessels and also, possibly, to cardiomyocytes. The aim of the present study was to determine whether stem cells are retained in the adult human and murine epicar...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.107.150755
更新日期:2007-12-07 00:00:00
abstract::Bone marrow-derived cells (BMCs) have been implicated as a modifiers of vascular growth either directly by transdifferentiation into endothelial cells (ECs) or indirectly through growth factor release. To examine these possibilities under physiological conditions, we developed a model of hypoxia-mediated angiogenesis ...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000189259.69645.25
更新日期:2005-11-11 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.108.182287
更新日期:2008-11-07 00:00:00
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更新日期:2011-10-14 00:00:00
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doi:10.1161/01.res.72.1.176
更新日期:1993-01-01 00:00:00
abstract:RATIONALE:Despite significant interest in bone marrow mononuclear cell (BMC) therapy for ischemic heart disease, current techniques have resulted in only modest benefits. However, selected patients have shown improvements after autologous BMC therapy, but the contributing factors are unclear. OBJECTIVE:The purpose of ...
journal_title:Circulation research
pub_type: 杂志文章,多中心研究,随机对照试验
doi:10.1161/CIRCRESAHA.116.304710
更新日期:2015-01-02 00:00:00
abstract::Cardiac failure appears rapidly during severe hypoxia and precedes a substantial reduction in adenosine triphosphate content. Reduced adenosine triphosphate turnover, in the presence of nearly normal content, may be the metabolic basis for contractile failure during hypoxia. To measure both the myocardial content and ...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.60.6.871
更新日期:1987-06-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.75.3.591
更新日期:1994-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.49.3.600
更新日期:1981-09-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.0000041418.51906.57
更新日期:2002-11-15 00:00:00
abstract:RATIONALE:Although the fibroblast growth factor (FGF) signaling axis plays important roles in heart development, the molecular mechanism by which the FGF regulates cardiogenesis is not fully understood. OBJECTIVE:To investigate the mechanism by which FGF signaling regulates cardiac progenitor cell differentiation. ME...
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pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.111.255950
更新日期:2012-02-17 00:00:00
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pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.108.192328
更新日期:2009-04-10 00:00:00
abstract::Fetal ventricular performance has been considered limited because ventricular output does not increase with rapid volume expansion above mean left atrial pressures (mLAPs) of 5-7 mm Hg. To explore relations between preload, afterload, and stroke volume (SV) in the fetal left ventricle, we instrumented 126-129 days ges...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.65.1.127
更新日期:1989-07-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/hh1201.091796
更新日期:2001-06-22 00:00:00
abstract::Myocardial damage due to reperfusion of ischemic tissue is caused primarily by infiltrating neutrophils. Although leukocyte beta2 integrins (CD18) play a critical role, significant neutrophil emigration persists when CD18 is neutralized or absent. This study examined the role of leukocyte beta1 integrin (alpha4) and i...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.0000013835.53611.97
更新日期:2002-03-22 00:00:00
abstract::To clarify the physiological role of calcium-activated neutral protease (CANP) in human platelets, we loaded the platelets with a Ca2+ -sensitive fluorescent dye, fura-2, and measured the degree of aggregation, cytosolic calcium ion concentration [( Ca2+]i), and proteolysis by sodium dodecyl sulfate-polyacrylamide gel...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.64.2.407
更新日期:1989-02-01 00:00:00
abstract::E1A can evoke G1 exit in cardiac myocytes and other cell types by displacing E2F transcription factors from tumor suppressor "pocket" proteins and by a less well-characterized p300-dependent pathway. Bypassing pocket proteins (through overexpression of E2F-1) reproduces the effect of inactivating pocket proteins (thro...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.85.4.319
更新日期:1999-08-20 00:00:00
abstract:RATIONALE:We have shown recently that particulate (pGC) and soluble guanylyl (sGC) cyclases synthesize cGMP in different compartments in adult rat ventricular myocytes (ARVMs). OBJECTIVE:We hypothesized that cGMP-dependent protein kinase (PKG) exerts a feedback control on cGMP concentration contributing to its intrace...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.110.226712
更新日期:2010-11-12 00:00:00
abstract::We previously reported that hyperhomocysteinemia (HHcy), an independent risk factor of coronary artery disease (CAD), is associated with increased atherosclerosis and decreased plasma high-density lipoprotein cholesterol (HDL-C) in cystathionine beta-synthase-/apolipoprotein E-deficient (CBS(-/-)/apoE(-/-)) mice. We o...
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pub_type: 杂志文章
doi:10.1161/01.RES.0000242559.42077.22
更新日期:2006-09-15 00:00:00
abstract::[3H](+/-)Carazolol, a newly available beta-adrenergic receptor antagonist, can be used to characterize beta-adrenergic receptor subtypes present in membrane vesicles derived from canine ventricular myocardium and canine lung. [3H](+/-)Carazolol binding is saturable, of high affinity, and is displaceable by beta-adrene...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.49.2.326
更新日期:1981-08-01 00:00:00
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pub_type: 杂志文章,评审
doi:10.1161/RES.0000000000000110
更新日期:2016-08-19 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章,评审
doi:10.1161/01.res.36.6.107
更新日期:1975-06-01 00:00:00
abstract:RATIONALE:Hydroxymethyl glutaryl-coenzyme A reductase degradation protein 1 (Hrd1) is an endoplasmic reticulum (ER)-transmembrane E3 ubiquitin ligase that has been studied in yeast, where it contributes to ER protein quality control by ER-associated degradation (ERAD) of misfolded proteins that accumulate during ER str...
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pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.115.306993
更新日期:2015-08-28 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000104084.88317.91
更新日期:2003-11-28 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.46.5.720
更新日期:1980-05-01 00:00:00
abstract::The sinoatrial node, which resides at the junction of the right atrium and the superior caval vein, contains specialized myocardial cells that initiate the heart beat. Despite this fundamental role in heart function, the embryonic origin and mechanisms of localized formation of the sinoatrial node have not been define...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000258019.74591.b3
更新日期:2007-02-16 00:00:00
abstract:RATIONALE:Thousands of mutations across >50 genes have been implicated in inherited cardiomyopathies. However, options for sequencing this rapidly evolving gene set are limited because many sequencing services and off-the-shelf kits suffer from slow turnaround, inefficient capture of genomic DNA, and high cost. Further...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.115.306723
更新日期:2015-09-11 00:00:00
abstract::The mechanism(s) by which mutations in sarcomeric proteins cause hypertrophic cardiomyopathy (HCM) remains unknown. A leading hypothesis proposes that mutant sarcomeric proteins impair cardiac myocyte contractility, providing an impetus for compensatory hypertrophy. To test this hypothesis, we determined the impact of...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.81.1.76
更新日期:1997-07-01 00:00:00
abstract::Bone morphogenetic protein receptor 2 (BMPR2) mutations have been linked to familial pulmonary arterial hypertension (PAH), but the molecular pathways leading to this severe pathology remain poorly characterized. We report that hypoxia, a paramount stimulus for the development of pulmonary hypertension, suppresses the...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000237021.65103.24
更新日期:2006-08-04 00:00:00