A1D-Adrenergic receptors

Perez DM, Piascik MT, Graham RM. Solution-phase library screening for the identification of rare clones isolation of an a1D adrenergic receptor cDNA. Mol Pharmacol 1991 40 876-883. 

Tanoue A, Nasa Y, Koshimizu T, et al. The a1D-adrenergic receptor directly regulates arterial blood pressure via vasoconstriction. J Clin Invest 2002 109 765-775. 

Perez DM, DeYoung MB, Graham RM. Coupling of expressed a1B- and a1D-adrenergic receptor to multiple signaling pathways is both G protein and cell type specific. Mol Pharmacol 1993 44 784-795. 

Carrieri A, Centeno NB, Rodrigo J, Sanz F, Carotti A. Theoretical evidence of a salt bridge disruption as the initiating process for the a1D-adrenergic receptor activation a molecular dynamics and docking study. Proteins 2001 43 382-394. 

Hague C, Chen Z, Pupo AS, Schulte N, Toews ML, Minneman KP. The N-termi-nus of the human a1D-adrenergic receptor prevents cell surface expression. J Pharm Exp Ther 2004 309 388-397. 

Sands SA, Morilak DA. Expression of a1D adrenergic receptor messenger RNA in oxytocin- and corticotropin-releasing hormone-synthesizing neurons in the rat paraventricular nucleus. Neuroscience 1999 91 639-649. 

Williams AM, Nguyen ML, Morilak DA. Co-localization of a1D adrenergic receptor mRNA with mineralocorticoid and glucocorticoid receptor mRNA in rat hippocampus. J Neuroendocrinol 1997 9 113-119. 

Chu CP, Kunitake T, Kato K, et al. The a1D-adrenergic receptor modulates cardiovascular and drinking responses to central salt loading in mice. Neurosci Lett 2004 356 33-36. 

Tanoue A, Koba M, Miyawaki S, et al. Role of the a1D-adrenergic receptor in the development of salt-induced hypertension. Hypertension 2002 40 101-106. 

Harasawa I, Honda K, Tanoue A, et al. Responses to noxious stimuli in mice lacking a1D adrenergic receptors. Neuroreport 2003 14 1857-1860. 

Selected Gene Expression Changes in Epinephrine-Stimulated Rat-1 Fibroblasts Expressing a1A-, a1B-, or a1D-Adrenergic Receptors... 

Of the nine adrenergic receptor subtypes, the a1D is the only one to be identified by cloning before characterization pharmacologically. Subsequently, it was shown that the so-called alc-receptor was actually the pharmacological a1A (64,65), and this was formalized by the IUPHAR Adrenergic Receptor Subcommittee (66). The current classification scheme includes the a1A, a1B, and a1D, but there is no alc. A fourth pharmacological subtype, the a1L, has been identified in vascular tissues from several species (67) but may represent a conformational state of the a1A-receptor (68). 

Mice lacking the oqB-adrenergic receptor were generated by the Cotecchia lab in 1997 (76). Whereas basal blood pressure was not altered in these animals, the hypertensive response to oq-agonists was significantly blunted. Subsequently, the a1A- (77) and a1D-knockouts (78) were generated. All three oq-subtypes play important roles in the cardiovascular system, and the oqB may be particularly important in the central nervous system (reviewed in ref. 79) (see Chapter 8). 

Hague C, Uberti M, Chen Z, Hall RA, Minneman KP. Cell surface expression of a1D-ARs is controlled by heterodimerization with a, B-adrenergic receptors. J Biol Chem 2004 279 15,541-15,549. 

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