Background
Previous work demonstrated that maternal haplotypes of the β2-adrenoceptor gene (ADRB2) influence ephedrine requirements during cesarean delivery. The use of ephedrine versus a pure α-adrenergic agonist such as phenylephrine has been associated with lower umbilical artery (UA) pH, thought to be secondary to increased fetal metabolism. There are no data evaluating the effect of fetal/neonatal genotypes on the metabolic response to maternally administered vasopressors. We hypothesized that neonatal ADRB2 genotype would affect the extent of neonatal acidemia. We also examined the effect of maternal ADRB2 and the endothelial nitric oxide synthase gene (NOS3) on ephedrine and phenylephrine requirements for treatment of maternal hypotension.

The effect of maternal and fetal β2-adrenoceptor and nitric oxide synthase genotype on vasopressor requirement and fetal acid-base status during spinal anesthesia for cesarean delivery.

Interactions between the genes of vasodilatation pathways influence blood pressure and nitric oxide level in hypertension.

BACKGROUND The β2-adrenoceptor (ADRB2 gene) possesses several polymorphic sites that have physiologic and/or pharmacologic significance. Previous work has demonstrated that the ADRB2 genotype affects the amount of ephedrine administered to maintain blood pressure during cesarean delivery with spinal anesthesia. This study investigated whether the ADRB2 genotype affected phenylephrine dose requirements during cesarean delivery. Our hypothesis was that the ADRB2 genotype altered the ephedrine dose-response and that we would not see this effect if phenylephrine was the vasopressor used to maintain blood pressure because phenylephrine does not act via the β2-adrenoceptor. METHODS Women undergoing elective cesarean delivery were studied. Baseline systolic blood pressure (SBP) was determined, and spinal anesthesia was initiated with hyperbaric bupivacaine 12 mg, fentanyl 20 μg, and morphine 200 μg. Hypotension was treated with a phenylephrine infusion using a standardized algorithm (50 μg/min if SBP was 90%-99% of baseline, 100 μg/min for SBP 80%-89% baseline, and 200 μg/min plus boluses for SBP <80% baseline) for 15 minutes after the administration of spinal anesthesia. ADRB2 genotype at codons 16 and 27 was determined. The effect of genotype on administered phenylephrine was compared by analysis of variance and linear regression. RESULTS Ninety-six women completed the protocol with full data available for analysis. In the unadjusted analysis, there were no significant differences in phenylephrine dose administered among different genotypes at codons 16 and 27. When adjusted for covariates (maternal body mass index, baseline systolic and diastolic blood pressure, neonatal weight, and ethnicity), there was an increase of 200 μg (95% confidence interval, 4-396; P = 0.04) in phenylephrine administered to Arg16 homozygous genotype subjects compared with Gly16 homozygous genotype subjects. CONCLUSIONS Phenylephrine dose requirements to maintain SBP after spinal anesthesia are affected by ADRB2 genotype but to a lesser extent than ephedrine. This suggests that previous work demonstrating a large effect of ADRB2 genotype on ephedrine dose requirements may be explained, at least in part, by a differential response to ephedrine based on ADRB2 genotype. It also suggests that there may be ADRB2-mediated differences in the physiologic response to spinal anesthesia.

The Effect of β2-Adrenoceptor Genotype on Phenylephrine Dose Administered During Spinal Anesthesia for Cesarean Delivery.

Aims: β-Adrenergic receptors (ADRBs) play a pivotal role in cardiovascular disease. Recently, genetic polymorphisms of ADRB1 and ADRB2 have been suggested to be associated with cardiovascular event...

β2-Adrenergic Receptor Gene Polymorphisms Are Associated with Cardiovascular Events But not All-Cause Mortality in Coronary Artery Disease Patients: A Meta-Analysis of Prospective Studies

Background. Beta2-adrenergic receptor (ADRB2) gene polymorphisms, Arg16Gly and Gln27Glu, have been implicated in the pathogenesis of cardiovascular diseases. The aim of this study was to determine the association of these two polymorphisms with the risk of myocardial infarction (MI) in the Egyptian population. Methods. Blood samples were collected from 68 MI patients and 75 healthy controls. They were assessed for the presence of cardiovascular risk factors and genotyped for the Arg16Gly (rs1042713) and Gln27Glu (rs1042714) polymorphisms using allelic-discrimination polymerase chain reaction. Results. There is no significant difference in genotype and allele frequencies at codon 16 between MI patients and controls (). However, at codon 27, MI risk was higher in Gln27 homozygous participants than in Glu27 carriers (). The haplotype frequency distribution showed significant difference among cases and controls (); homozygotes for Gly16/Gln27 haplotype were more susceptible to MI than Gly16/Glu27 carriers. Patients with Arg16/Gln27 haplotype had higher serum total cholesterol levels () and lower frequency of diabetes in MI patients (). However, both Glu27 genotypes and haplotype showed lower frequency of hypertension (). Conclusions. Our findings suggested that the ADRB2 gene polymorphisms may play an important role in susceptibility of MI among Egyptian population.

/pdf/beta2-adrenergic-receptor-gene-polymorphisms-in-egyptian-3aw3efmfql.pdf

Beta2-Adrenergic Receptor Gene Polymorphisms in Egyptian Patients with Acute Myocardial Infarction

Genetic variation in drug targets (e.g. receptors) can have pronounced effects on clinical responses to endogenous and exogenous agonists. Polymorphisms in the gene encoding the β(2)-adrenergic receptor (β(2)-AR) have been associated with altered expression, down-regulation, and altered cell signaling in vitro. Because β(2)-ARs play a crucial role in the regulation of the cardiovascular system, the functional importance of genetic variation in the β(2)-AR on cardiovascular responses to physiological or pharmacological stimuli has gained widespread attention. The objective of this review is to characterize these intermediate cardiovascular phenotypes and their influence on cardiovascular disease and adrenergic drug responses.Two common single nucleotide polymorphisms, encoded at codon 46 (Gly(16)Arg) and 79 (Gln(27)Glu) of the β(2)-AR gene, have been studied intensively. They have been shown to be associated with altered vasodilator responses to regional and systemic administration of β(2)-agonists, altered cardiovascular responses to sympathoexcitatory maneuvers, and altered myocardial function. Importantly, these intermediate physiological patterns may influence the development of and the outcomes associated with hypertension and other cardiovascular diseases. As recently reported, β(2)-AR gene variation can risk-stratify patients receiving β-blocker therapy and may predict β-blocker efficacy in patients post acute coronary syndrome or in patients with heart failure.Further studies will advance our understanding of the link between β(2)-AR genotypes, intermediate cardiovascular phenotypes, and clinical phenotypes. In the long term, reassessment of the benefits of β-blocker-therapy within genotype groups should be carried out with the ultimate goal to design the optimal therapeutic regimen for the individual patient.

/pdf/genetic-variation-in-the-b2-adrenergic-receptor-impact-on-314gwxv7bu.pdf

GENETIC VARIATION IN THE β2-ADRENERGIC RECEPTOR: IMPACT ON INTERMEDIATE CARDIOVASCULAR PHENOTYPES

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GENETIC VARIATION IN THE β2-ADRENERGIC RECEPTOR: IMPACT ON INTERMEDIATE CARDIOVASCULAR PHENOTYPES