Home LiteratureArticle Details
PMID: 9570482 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

N- and C-terminal structure-activity study of angiotensin II on the angiotensin AT2 receptor.

European journal of pharmacology ·Vol. 343 ·No. 2-3 ·1998-02-19 ·Pages 323-31

Bouley R, Pérodin J, Plante H, Rihakova L, Bernier SG, Maletínská L, Guillemette G, Escher E

Abstract

The predominant angiotensin II receptor expressed in the human myometrium is the angiotensin AT2 receptor. This preparation was used for a structure-activity relationship study on angiotensin II analogues modified in positions 1 and 8. The angiotensin AT2 receptor present on human myometrium membranes displayed a high affinity (pKd = 9.18) and was relatively abundant (53-253 fmol/mg of protein). The pharmacological profile was typical of an angiotensin AT2 receptor with the following order of affinities: (angiotensin III > or = angiotensin II > angiotensin I > PD123319 > angiotensin-(1-7) > angiotensin-(1-6) approximately angiotensin IV >> Losartan). Modifications of the N-terminal side chain and of the primary amine of angiotensin II were evaluated. Neutralisation of the methylcarboxylate (Asp) to a methylcarboxamide (Asn) or to a hydroxymethyl (Ser) or substitution for a methylsulfonate group (cysteic acid) improved the affinity. Extension from methylcarboxylate (Asp) to ethylcarboxylate (Glu) did not affect the affinity. Introduction of larger side chains such as the bulky p-benzoylphenylalanine (p-Bpa) or the positively charged Lys did not substantially affect the affinity. Complete removal of the side chain (angiotensin III), however, resulted in a significant affinity increase. Removal or acetylation of the primary amine of angiotensin II did not noticeably influence the affinity. Progressive alkylation of the primary amine significantly increased the affinity, betain structures being the most potent. It appears that quite important differences exist between the angiotensin AT1 and AT2 receptors concerning their pharmacological profile towards analogues of angiotensin II modified in position 1. On position 8 of angiotensin II, a structure-activity relationship on the angiotensin AT2 receptor was quite similar to that observed with angiotensin AT1 receptor. Bulky, hydrophobic aromatic residues displayed affinities similar to or even better than [Sarcosine1]angiotensin II. Aliphatic residues, especially those of reduced size, caused a significant decrease in affinity especially [Sarcosine1, Gly8]angiotensin II who showed a 30-fold decrease. Introduction of a positive charge (Lys) at position 8 reduced the affinity even further. Stereoisomers in position 8 (L-->D configuration) also induced lower affinities. The angiotensin AT2 receptor display a structure-activity relationship similar to that observed on the AT1 receptor for the C-terminal position of the peptide hormone. Position 1 structure-activity relationships are however fundamentally different between the angiotensin AT1 and AT2 receptor.

MeSH Terms
Angiotensin II/chemistry,metabolism,pharmacology Binding Sites Female Humans In Vitro Techniques Myometrium/metabolism Receptors, Angiotensin/drug effects,metabolism Structure-Activity Relationship
Chemicals
Receptors, Angiotensin Angiotensin II
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Bouley R
Département de Pharmacologie, Faculté de Médecine, Université de Sherbrooke, Que., Canada.
Pérodin J
Plante H
Rihakova L
Bernier S G
Maletínská L
Guillemette G
Escher E
Article Info
Journal
European journal of pharmacology
Abbr.
Eur J Pharmacol
ISSN
0014-2999
Published
1998-02-19
Pages
323-31
Language
English
Region
Netherlands
NLM ID
1254354
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]