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A dicarba analog of β‐atrial natriuretic peptide (β‐ANP) inhibits guanosine 3′,5′‐cyclic monophosphate production induced by α‐ANP in cultured rat vascular smooth muscle cells
Author(s) -
Kambayashi Yoshikazu,
Nakajima Shigeyuki,
Ueda Motohiko,
Inouye Ken
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80425-9
Subject(s) - atrial natriuretic peptide , vascular smooth muscle , cyclic guanosine monophosphate , medicine , chemistry , endocrinology , guanosine , intracellular , biology , biochemistry , smooth muscle , nitric oxide
The synthesis and biological properties are described of [Asu 7,23′ ]‐β‐ANP‐(7–28) (Asu, L‐α‐aminosuberic acid), a dicarba analog of β‐atrial natriuretic peptide (β‐ANP, an antiparallel dimer of human α‐ANP with the chains linked by 7–23′ and 7′–23 disulfide bonds). This Asu‐analog (referred to as analog III) displaced 125 I‐α‐ANP specifically bound to cultured rat vascular smooth muscle cells (VSMC) with an apparent K i of 2.1 × 10 −8 M, but did not stimulate formation of intracellular cGMP at 10 −8 –10 −5 M. Analog III inhibited the α‐ANP‐stimulated cGMP production in VSMC competitively with a p A 2 value of 7.45 and behaved as an antagonist of α‐ANP in rat aorta smooth muscle relaxation. In addition, β‐ANP was also shown to inhibit the α‐ANP‐induced cGMP production in a dose‐dependent manner. The mechanism of action of β‐ANP is also discussed.