(Hypertension. 1995;25:924-927.)
© 1995 American Heart Association, Inc.
Articles |
Proposed Update of Angiotensin Receptor Nomenclature
From the IUPHAR Nomenclature Subcommittee for Angiotensin Receptors.
Correspondence to Marc de Gasparo, MD, Research Department, Pharmaceuticals Division, Ciba-Geigy Ltd, 4002 Basel, Switzerland.
Key Words: nomenclature • angiotensin II • renin-angiotensin system • receptors, angiotensin II • radioligand assay • losartan
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Introduction |
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Angiotensin II exerts a wide range of actions on the heart, blood vessels, adrenals, kidneys, and nervous system and plays a major role in blood pressure maintenance and volume homeostasis. Its effects are mediated mainly by plasma membrane receptors. Efforts to elucidate the nature and distribution of these receptors have involved intensive research on the part of pharmacologists, molecular biologists, and clinicians, and to avoid confusion it is therefore important that a uniform nomenclature be adopted by all disciplines concerned. The International Union of Pharmacology (IUPHAR) Nomenclature Subcommittee for Angiotensin Receptors met in Oxnard, Calif, in February 1994. At this meeting, scientists working in the field were invited to exchange views on new issues relating to angiotensin receptor subtypes, their functions, and appropriate amendments to the nomenclature proposed in 1991.1 The committee has not yet been able to put forward a definitive recommendation in this fast-moving area, but the simple and workable guidelines suggested in this article reflect the opinion of many specialists. Comments from the scientific community are welcome to help in formulating a proposal that could be endorsed by the IUPHAR.
To avoid any ambiguity, it is recommended that Ang should be used as the standard abbreviation for the hormone angiotensin, in conformity with a previous report2 from the Joint Nomenclature and Standardization Committee of the International Society of Hypertension, American Heart Association, and the World Health Organization published in the Journal of Hypertension in 1987. The abbreviation AT is misleading. The amino acid sequence of human [Ile5]angiotensin-(1-10) decapeptide (Ang I) serves as reference for all angiotensin peptides, and the numbering of the amino acids follows that of human Ang I. Fragments of angiotensin and analogues are defined in the same manner as those of human Ang I, eg, Ang-(3-8) (now called Ang IV), with the sequence Val-Tyr-Ile-His-Pro-Phe.
The angiotensin receptor is abbreviated AT, and its subtypes are identified by the subscripts 1, 2, and so on, in line with the earlier proposals.1 Following common usage, the species should be stated first, eg, human AT1 or rat AT2. When convincing evidence can be adduced for further subdivision of the AT1 and AT2 receptors, the subscript suffixes A, B, C, and so on should be used (eg, AT1A). The lowercase subscript letter should be used for recombinant receptors defined by molecular biology3 and the uppercase subscript letter reserved for pharmacologically defined receptor subtypes.3 As soon as the pharmacology of a recombinant receptor is known, the subscript should be capitalized. The use of at1 and at2 in lowercase is recommended when referring to the gene whose product displays pharmacological characteristics close to those of the native receptor protein.
Mammalian Ang II receptors have been classified according to the following three criteria: (1) binding of natural ligand, eg, Ang II, Ang III, Ang IV; (2) selectivity of prototypical ligands, as described earlier,1 eg, for AT1: losartan and similar antagonists (valsartan, L-158,809, GR 117289, SK&F 108566, TCV-116, SR 47436, etc) and for AT2: PD 123177, PD 123319, CGP 42112, etc; and (3) structure and properties.
Although these criteria have been considered to afford a useful working framework, more and more new information is becoming available, mainly with regard to molecular biology. It therefore appears desirable to adopt the IUPHAR recommendation in devising a useful integrated receptor classification scheme reconciling operational data with structural data. The three main criteria proposed by the IUPHAR4 are (1) operational, ie, drug-related characteristics (selective agonists and antagonists, ligand binding affinities); (2) transductional, ie, receptor-effect coupling events; and (3) structural, ie, gene and receptor sequence. Provided all three criteria are addressed, it should be possible to obtain a "fingerprint" capable of identifying distinct receptors.4
AT1 and AT2 Receptors
For the time being, the subcommittee proposes to classify
mammalian receptors into two major subgroups, AT1 and
AT2, as shown in Tables 1 through 3.
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Other Receptors
The AT3 subtype described by Chaki and
Inagami30 in the neuro 2A neuroblastoma cell line is
peptide specific: It recognizes Ang II but has a negligible affinity
for Ang III. This subtype has no affinity for nonpeptide ligands such
as losartan or PD 123319. It has been observed only in cell lines. This
binding site stimulates soluble guanylate cyclase by a nitric
oxide–mediated process.31 The AT3 subtype
requires further characterization. In this particular case, and in
general when the receptor is not typically AT1 or
AT2, it is preferable to use the common term AT,
with the indication of the species, tissue, or cell line, eg, neuro 2A
AT.
It is proposed that AT4 should be used for the new receptor for which Ang IV (Ki<1 nmol/L)32 33 is the natural ligand. This binding site is distributed in a variety of tissues, including heart, lung, kidney, brain, and liver. It has no affinity for losartan or PD 123319. It could be involved in cerebral and renal cortical blood flow and could enhance cognitive functions. No nonpeptidic ligand for this binding site has been described so far. The sequence and transducing mechanism are also unknown.34 35 36
As the pharmacology of AT3 and AT4 is not yet sufficiently well characterized, they are not yet included in a definitive broad classification of mammalian AT receptors.
Mutant receptors should be so designated as to specify the position of the amino acid substitution. For example, [L112P] AT1a would indicate that leucine in position 112 has been replaced by proline for the AT1a receptor.
Nonmammalian receptors should be classified separately, as they may not have the same characteristics as the mammalian receptors: Xenopus AT receptors have the functional properties of the mammalian AT1 receptor but recognize CGP 42112 and do not significantly bind losartan or PD 123319.37 Ang II binding sites have also been described in microorganisms such as Mycoplasma.38 39
Although this classification is likely to evolve further, these simple rules will be helpful in avoiding confusion among investigators. The combined application of the operational, transductional, and structural criteria should prevent new names being given to receptors that are species-homologous and only slightly different from the AT1 and AT2 receptors already described.
Chemical Names
AT1 Receptor
Losartan:
2-n-butyl-4-chloro-5-(hydroxymethyl)-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]imidazole;
valsartan:
(S)-N-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]-methyl]-valine;
L-158,809:
5,7-dimethyl-2-ethyl-3-[[2-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]imidazol[4,5-b]pyridine;
GR 117289:
(1-[[3-bromo-2-[2-(1H-tetrazol-5-yl)phenyl]-5-benzofuranyl]methyl]-2-butyl-4-chloro-1H-imidazole-5-carboxylic
acid); SK&F 108566:
(E)-3-[2-butyl-1-(4-carboxybenzyl)-1H-imidazol-5-yl]-2-[(2-thienyl)methyl]propenoic
acid; TCV-116: (±)-1-[[(cyclohexyloxy)carbonyl]oxy]ethyl
2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]-1H-benzimidazole-7-carboxylate;
SR 47436:
(2-n-butyl-4-spirocyclopentane-1-((2'-(1H-tetrazol-5-yl)biphenyl-4-yl)-4,5-dihydro-1H-imidazole-5-one).
AT2 Receptor
PD 123177:
1-[(4-amino-3-methylphenyl)methyl]-5-(dephenylacetyl)-4,5,6,7-tetrahydro-1H-imidazol[4,5-c]pyridine-6-carboxylic
acid; PD 123319:
(S)-1-[[4-(di-methylamino)-3-methylphenyl]methyl]-5-(diphenylacetyl)-4,5,6,7-tetrahydro-1H-imidazol[4,5-c]pyridine-6-carboxylic
acid; CGP 42112:
nicotinyl-Tyr-(N
-benzyloxycarbonyl-Arg)Lys-His-Pro-Ile-OH.
Received October 6, 1994; first decision November 7, 1994; accepted January 3, 1995.
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References |
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Y. Mori, H. Matsubara, S. Murasawa, K. Kijima, K. Maruyama, H. Tsukaguchi, N. Okubo, T. Hamakubo, T. Inagami, T. Iwasaka, et al. Translational Regulation of Angiotensin II Type 1A Receptor: Role of Upstream AUG Triplets Hypertension, November 1, 1996; 28(5): 810 - 817. [Abstract] [Full Text]
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 F. H. Messerli, M. A. Weber, and H. R. Brunner Angiotensin II Receptor Inhibition: A New Therapeutic Principle Arch Intern Med, September 23, 1996; 156(17): 1957 - 1965. [Abstract] [PDF]
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P. Gohlke, W. Linz, B. A. Scholkens, G. Wiemer, and T. Unger Cardiac and Vascular Effects of Long-term Losartan Treatment in Stroke-Prone Spontaneously Hypertensive Rats Hypertension, September 1, 1996; 28(3): 397 - 402. [Abstract] [Full Text]
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L. A. Sechi, C. A. Griffin, G. Giacchetti, J.-P. Valentin, C. Llorens-Cortes, P. Corvol, and M. Schambelan Tissue-Specific Regulation of Type 1 Angiotensin II Receptor mRNA Levels in the Rat Hypertension, September 1, 1996; 28(3): 403 - 408. [Abstract] [Full Text]
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 T. L. Goodfriend, M. E. Elliott, and K. J. Catt Angiotensin Receptors and Their Antagonists N. Engl. J. Med., June 20, 1996; 334(25): 1649 - 1655. [Full Text] [PDF]
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M. Ye, G. Flores, and D. Batlle Angiotensin II and Angiotensin-(1-7) Effects on Free Cytosolic Sodium, Intracellular pH, and the Na+-H+ Antiporter in Vascular Smooth Muscle Hypertension, January 1, 1996; 27(1): 72 - 78. [Abstract] [Full Text]
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 A. L. Albiston, S. G. McDowall, D. Matsacos, P. Sim, E. Clune, T. Mustafa, J. Lee, F. A. O. Mendelsohn, R. J. Simpson, L. M. Connolly, et al. Evidence That the Angiotensin IV (AT4) Receptor Is the Enzyme Insulin-regulated Aminopeptidase J. Biol. Chem., December 21, 2001; 276(52): 48623 - 48626. [Abstract] [Full Text] [PDF]
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