ArticleBritish journal of pharmacology2000
Splice isoforms of alpha(1a)-adrenoceptor in rabbit.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 32 citations in OpenAlex.
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- Identification and profiling of novel α1A-adrenoceptor-CXC chemokine receptor 2 heteromer.The Journal of biological chemistry · 2012Article
- Phenotype pharmacology of lower urinary tract α(1)-adrenoceptors.British journal of pharmacology · 2012Review
- What makes the α(1A)-adrenoceptor gene express the α(1L)-adrenoceptor functional phenotype?British journal of pharmacology · 2012Article
- Novel drug targets for the pharmacotherapy of benign prostatic hyperplasia (BPH).British journal of pharmacology · 2011Review
- The alpha1A-adrenoceptor gene is required for the alpha1L-adrenoceptor-mediated response in isolated preparations of the mouse prostate.British journal of pharmacology · 2008Article
- Alpha-1 adrenoceptor up-regulation induced by prazosin but not KMD-3213 or reserpine in rats.British journal of pharmacology · 2002Article
- Distribution of alpha-1 adrenoceptor subtypes in RNA and protein in rabbit eyes.British journal of pharmacology · 2002Article
- Inverse agonism and neutral antagonism at a constitutively active alpha-1a adrenoceptor.British journal of pharmacology · 2000Article
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5 authors at 1 institution in 1 country.
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Abstract
Two splice isoforms of rabbit alpha(1a)-adrenergic receptor (AR), (named alpha(1a)-OCU.2-AR and alpha(1a)-OCU.3-AR) have been isolated from the liver cDNA library in addition to the previously reported isoform (alpha(1a)-OCU.1-AR). Although they have the identical splice position with human alpha(1a)-AR isoforms, the C-terminal sequences are distinct from those of human isoforms. Among these rabbit alpha(1a)-AR isoforms, there are no significant differences in pharmacological properties: high affinity for prazosin, WB4101, KMD-3213 and YM617 and low affinity for BMY7378, using COS-7 cells expressing each isoform by radioligand binding assay. Competitive reverse transcription-polymerase chain reaction (RT - PCR) analysis revealed that mRNA of alpha(1a)-ARs was expressed in liver, thoracic aorta, brain stem and thalamus of rabbit. The splice isoforms exhibited a distinct distribution pattern in rabbit; alpha(1a)-OCU. 1-AR was expressed most abundantly in those tissues. CHO clones, stably expressing each isoforms with receptor density 740 fmol mg(-1) protein in alpha(1a)-OCU.1-AR, 1200 fmol mg(-1) in alpha(1a)-OCU.2-AR and 570 fmol mg(-1) in alpha(1a)-OCU.3-AR, respectively, showed a noradrenaline-induced increase in inositol trisphosphate which was suppressed by prazosin. Noradrenaline elicited a concentration-dependent increase in extracellular acidification rate (EAR) in the CHO clones with pEC(50) values of 6. 19 for alpha(1a)-OCU.1-AR, 6.49 for alpha(1a)-OCU.2-AR and 6.58 for alpha(1a)-OCU.3-AR, respectively. Noradrenaline caused a concentration-dependent increase in intracellular Ca(2+) concentration ([Ca(2+)]i) in the CHO clones with pEC(50) values of 6. 14 for alpha(1a)-OCU.1-AR, 7.25 for alpha(1a)-OCU.2-AR and 7.70 for alpha(1a)-OCU.3-AR, respectively. In conclusion, the present study shows the occurrence of three splice isoforms of rabbit alpha(1a)-AR, which are unique in C-terminal sequence and in tissue distribution. They show similar pharmacological profiles in binding studies but alpha(1a)-OCU.3-AR had the highest potency of noradrenaline in functional studies in spite of the lowest receptor density. These findings suggest that the structure of C-terminus of alpha(1a)-ARs may give the characteristic functional profile.
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