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The impact of β2-adrenergic receptor polymorphism in asthma and congestive heart failure
Journal of Pharmaceutical Care & Health Systems

Journal of Pharmaceutical Care & Health Systems
Open Access

ISSN: 2376-0419

The impact of β2-adrenergic receptor polymorphism in asthma and congestive heart failure


Pharmaceutical Summit and Expo

October 08-10, 2015 New Delhi, India

Jose Sanesh Prasad, Samanta Malay Kumar, Arun Kanniyappan Parthasarathy and Thomas Abhilash

J.S.S. University, India

Posters-Accepted Abstracts: J Pharma Care Health Sys

Abstract :

The ?²2-Adrenergic Receptor (ADRB2) is a member of the G-protein-coupled adrenergic receptor family with seven transmembrane segments. Similar to other members of this receptor family, beta2-AR specifically binds and is activated by the endogenous class of ligands known as catecholamines, and epinephrine in particular. The gene encoding this receptor, ADRB2, was cloned by Kobilka et al. in 1987 and is localized to chromosome 5q31â??q32, a region that has been linked with asthma and asthma related phenotypes. ADRB2 consists of a single exon of 2015 nucleotides, which encodes a 413 amino acid protein. This review highlights the genetic polymorphisms in ADRB2 and the pivotal role of beta2- AR in the regulation of the cardiac, pulmonary, vascular, endocrine, and central nervous systems. ADRB2 is abundantly expressed in bronchial smooth muscle cells and activation of the resulting receptor leads to bronchodilation. Beta2-AR is the target of clinically important drugs for asthma and cardiovascular conditions including hypertension and congestive heart failure (CHF). Beta-receptor agonists (e.g. albuterol, salmeterol) and antagonists (e.g. carvedilol and propranolol) are among the most commonly prescribed medications in the treatment of asthma and cardiovascular disease, respectively. A number of genetic polymorphisms in the ADRB2 gene have been described which affect gene expression, the function of the resulting receptor, and response to beta2-agonists.

Biography :

Email: [email protected]

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