Autonomic Nervous System Pharmacogenomics: A Progress Report

Kirstein, Shelli L.; Insel, Paul A.

doi:10.1124/pr.56.1.2

Cited by 133 publications

(140 citation statements)

References 233 publications

(318 reference statements)

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“…Numbers at the bottom of the column number of patients studied. Modified from Leineweber et al (2005) "loss-of-function" polymorphism with the Arg389 β-1 AR exhibiting a three-to fourfold higher isoprenaline-stimulated adenylyl cyclase activity than the Gly389 β-1 AR variant due to a better coupling of the Arg389 to G s -protein than the Gly389 β-1 AR variant (for recent reviews, see Small et al 2003;Leineweber et al 2004;Kirstein and Insel 2004;Brodde et al 2006).…”

Section: Possible Role Of β-1 Adrenoceptor Polymorphismsmentioning

confidence: 99%

“…Data obtained, however, are rather inconsistent; at present, it seems to be clear that these β-1 AR polymorphisms are not causally linked to cardiovascular diseases (are not disease-causing genes). They might, however, be involved in modifying progression of diseases and may affect drug responses (Small et al 2003;Kirstein and Insel 2004;Leineweber et al 2004;Brodde et al 2006). Thus, recent data indicate that the Arg389Gly β-1 AR polymorphism determines cardiac responses to dobutamine: dobutamine-infusion-evoked increases in heart rate and/or contractility were significantly larger in subjects homozygous for the Arg389 β-1 AR than in subjects with one or two Gly389 alleles (LaRosee et al 2004;Bruck et al 2005).…”

Section: Possible Role Of β-1 Adrenoceptor Polymorphismsmentioning

confidence: 99%

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β-adrenoceptor blocker treatment and the cardiac β-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure

Brodde

2007

Naunyn-Schmied Arch Pharmacol

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Section: Possible Role Of β-1 Adrenoceptor Polymorphismsmentioning

confidence: 99%

Section: Possible Role Of β-1 Adrenoceptor Polymorphismsmentioning

confidence: 99%

β-adrenoceptor blocker treatment and the cardiac β-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure

Brodde

2007

Naunyn-Schmied Arch Pharmacol

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“…Single nucleotide polymorphisms (SNPs) have now been found not only within the promoter region and the coding block [1] but also within the 3' untranslated region [2] of ADRB2. Additional studies have demonstrated that some of these polymorphisms may influence both receptor function and expression [1,3,4]. This could, potentially, impact quite heavily on how effectively agonists activate β 2 -adrenoceptors.…”

Section: Introductionmentioning

confidence: 99%

Influence of β2-adrenoceptor gene polymorphisms on β2-adrenoceptor expression in human lung

Kay

Suvarna

Scola

et al. 2010

Pulmonary Pharmacology & Therapeutics

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Background: The aim of the present study was to establish whether polymorphisms, especially those within the promoter region, of the β 2 -adrenoceptor gene (ADRB2) influence β 2 -adrenoceptor expression in human lung. Methods:The density of β-adrenoceptors in human lung tissue (n=88) was determined by saturation binding using the radioligand, iodinated cyanopindolol. Discrimination of β 1 -and β 2 -adrenoceptors was determined using the highly selective β 1 -adrenoceptor antagonist, CGP20712A. Genotype was determined at 5 positions of ADRB2 previously reported as polymorphic. Potential influences of single nucleotide polymorphisms (SNPs) within the promoter region (-367, -47) and coding block (46, 79, 491) of ADRB2 on β 2 -adrenoceptor expression were investigated. Results:The density of β 2 -adrenoceptors was variable among the 88 lung preparations studied ranging from 17 to 177 fmol/mg protein (mean±S.E.M., 72±4 fmol/mg protein).There was no influence of genotype on β 2 -adrenoceptor expression for any of the polymorphisms studied except at position 491. The polymorphism at position 491C>T, leading to a change from thr to ile at amino acid 164, is uncommon. Preparations genotyped as heterozygous (126±15 fmol/mg protein; n=5) expressed significantly (P = 0.0005) higher levels of β 2 -adrenoceptor than those that were homozygous (69±4 fmol/mg protein; n=83). M A N U S C R I P T A C C E P T E D ARTICLE IN PRESS

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“…The autonomic nervous system is responsible for homeostasis [1]. The preganglionic fibers of the sympathetic nervous system form synapses with sympathetic ganglia that are mediated by acetylcholine and its neuronal nicotinic receptor (nAChR [2]).…”

Section: Introductionmentioning

confidence: 99%

“…The preganglionic fibers of the sympathetic nervous system form synapses with sympathetic ganglia that are mediated by acetylcholine and its neuronal nicotinic receptor (nAChR [2]). This receptor is a pentamer formed by two alpha and three beta subunits (except the monomer formed only by alpha-7 subunits [1,2]). In sympathetic ganglia, alpha-3 is the predominant alpha subunit and, in association to beta-4 subunit, forms the "ganglia-type nAChR" [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Preservation of Alpha-3 Neuronal Nicotinic Acetylcholine Receptor Expression in Sympathetic Ganglia After Brain Death

et al. 2012

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The goal of this study was to evaluate if the immunohistochemical expression of alpha-3 neuronal nicotinic acetylcholine receptor subunit in sympathetic ganglia remains stable after brain death, determining the possible use of sympathetic thoracic ganglia from subjects after brain death as study group. The third left sympathetic ganglion was resected from patients divided in two groups: BDorgan donors after brain death and CON-patients submitted to sympathectomy for hyperhidrosis (control group). Immunohistochemical staining for alpha-3 neuronal nicotinic acetylcholine receptor subunit was performed; strong and weak expression areas were quantified in both groups. The BD group showed strong alpha-3 neuronal nicotinic acetylcholine receptor expression in 6.55% of the total area, whereas the CON group showed strong expression in 5.91% (p00.78). Weak expression was found in 6.47% of brain-dead subjects and in 7.23% of control subjects (p00.31). Brain death did not affect the results of the immunohistochemical analysis of sympathetic ganglia, and its use as study group is feasible.

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Autonomic Nervous System Pharmacogenomics: A Progress Report

Cited by 133 publications

References 233 publications

β-adrenoceptor blocker treatment and the cardiac β-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure

β-adrenoceptor blocker treatment and the cardiac β-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure

Influence of β2-adrenoceptor gene polymorphisms on β2-adrenoceptor expression in human lung

Preservation of Alpha-3 Neuronal Nicotinic Acetylcholine Receptor Expression in Sympathetic Ganglia After Brain Death

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