Overview
- Peptide (C)RPEPRGLPQ*SELNQE, corresponding to amino acid residues 160-174 of rat α2B-adrenoceptor with replacement of cysteine 169 (C169) with serine (*S) (Accession P19328). 2nd extracellular loop.
- Rat kidney, lung, liver lysates and rat skeletal muscle membrane (1:200).
- Western blot analysis of rat kidney (lanes 1 and 5), lung (lanes 2 and 6), liver (lanes 3 and 7) lysates and rat skeletal muscle membranes (lanes 4 and 8):1-4. Anti-α2B-Adrenergic Receptor (extracellular) Antibody (#AAR-021), (1:200).
5-8. Anti-α2B-Adrenergic Receptor (extracellular) Antibody, preincubated with α2B-Adrenergic Receptor (extracellular) Blocking Peptide (#BLP-AR021).
- Rat lung paraffin embedded sections (1:100).
- Cell surface detection of α2B-Adrenoreceptor by indirect flow cytometry in live intact mouse WEHI B-cell lymphoma cell line:___ Cells.
___ Cells + goat-anti-rabbit-FITC.
___ Cells + Anti-α2B-Adrenergic Receptor (extracellular) Antibody (#AAR-021), (5μg) + goat-anti-rabbit-FITC.
Adrenergic receptors (also called adrenoceptors) are the receptors for the catecholamines adrenaline and noradrenaline (called epinephrine and norepinephrine in the United States). Adrenaline and noradrenaline play important roles in the control of blood pressure, myocardial contractile rate and force, airway reactivity, and a variety of metabolic and central nervous system functions.
Adrenergic receptors are members of the G-protein coupled receptor (GPCR) superfamily of membrane proteins. They share a common structure of seven putative transmembrane domains, an extracellular amino terminus, and a cytoplasmic carboxyl terminus.
Adrenoceptors are divided into three types: α1, α2 and β-adrenoceptors. Each type is further divided into at least three subtypes: α1A, α1B, α1D, α2A, α2B, α2C, β1, β2, β31,2. Adrenoceptors are expressed in nearly all peripheral tissues and in the central nervous system1,2.
The α2B-adrenoceptor has a distinct pattern of expression within the brain, liver lung and kidney, and recent studies using the knock out mouse system have shown that disruption of this receptor indeed affects mouse viability3, blood pressure responses to α2-adrenoceptor agonists3 and the hypertensive response to salt loading4.
Like the α2A-adrenoceptor subtype, the α2B-adrenoceptor undergoes short term agonist promoted desensitization5. This desensitization is due to the phosphorylation of the receptor by G-protein coupled receptor kinases (GRKs)6 which ultimately promotes uncoupling of the receptor from the G-protein subunit7.