A dynorphin peptide induces hypotension by stimulating the release of atrial natriuretic peptide from rat atrium.
Intravenous injection of dynorphin A-(1-10) amide (Dyn, 81-324 nmol/kg) induced a dose-dependent hypotensive effect in the rat. This effect was antagonized by pretreatment with immunoglobulin G, purified from a specific antiserum raised against alpha-human atrial natriuretic peptide (anti-hANP-IgG), as well as by high doses of naloxone (2 or 10 mg/kg). In addition, a 12-fold increase in plasma level of atrial natriuretic peptide-like immunoreactivity (ANP-IR) was found following Dyn administration, which was accompanied by a significant decrease of atrial ANP-IR. These results suggest that the stimulated release of ANP-IR from the atrium may constitute one of the mechanisms for the depressor effect of dynorphin peptides.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004399:Dynorphins / Q000031:analogs & derivatives / Q000494:pharmacology*; D006325:Heart Atria / Q000187:drug effects / Q000378:metabolism; D007022:Hypotension / Q000139:chemically induced*; D007074:Immunoglobulin G / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D007074:Immunoglobulin G; D010446:Peptide Fragments; D004399:Dynorphins; C039666:dynorphin amide (1-10); D009320:Atrial Natriuretic Factor