What makes the α1A-adrenoceptor gene product assume an α1L-adrenoceptor phenotype?

Carl W. White, Edilson Dantas da Silva Junior, Linzi Lim, Sabatino Ventura

Research output: Contribution to journalReview articlepeer-review

3 Citations (Scopus)


The α1A-adrenoceptor is abundantly expressed in the lower urinary tract and is the principal therapeutic target for the symptomatic treatment of lower urinary tract symptoms in men. Prazosin has a lower affinity for the lower urinary tract α1A-adrenoceptor than α1A-adrenoceptors found in other parts of the body. This has led to the lower urinary tract α1A-adrenoceptor being subclassified as an α1L-adrenoceptor. It was demonstrated that this pharmacologically distinct α1L-adrenoceptor is a product of the α1A-adrenoceptor gene, but the mechanism by which this altered phenotype is achieved remains a mystery. Hypotheses for this altered pharmacology include the presence of an interacting protein such as cysteine-rich with EGF-like domain (CRELD) 1 or other GPCRs such as the CXCR2 chemokine or 5-HT1B receptor. Alternatively, the influence of breast cancer resistance protein (BCRP) efflux transporters on the pharmacology of α1A-adrenoceptors has also been investigated. These and other hypotheses will be described and discussed in this review. Linked Articles: This article is part of a themed section on Adrenoceptors—New Roles for Old Players. To view the other articles in this section visit https://onlinelibrary.wiley.com/doi/10.1111/bph.v176.14/issuetoc.

Original languageEnglish
Pages (from-to)2358-2365
Number of pages8
JournalBritish Journal of Pharmacology
Issue number14
Publication statusPublished - Jul 2019


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