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Peptide histidine isoleucine‐like immunoreactivity release from the rat gastric fundus
Author(s) -
Curró Diego,
Preziosi Paolo,
Ragazzoni Enzo,
Ciabattoni Giovanni
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb17023.x
Subject(s) - chemistry , radioimmunoassay , peptide , tetrodotoxin , endocrinology , medicine , microbiology and biotechnology , biochemistry , biology
1 Longitudinal muscle strips from the rat gastric fundus were subjected to in vitro electrical field stimulation (EFS) under non‐adrenergic non‐cholinergic (NANC) conditions to study the release of peptide histidine isoleucine‐like immunoreactivity (PHI‐LI) and the correlation between PHI‐LI release and NANC relaxation. 2 Different radioimmunoassay (RIA) systems employing C‐terminal‐ and N‐terminal‐specific anti‐PHI sera were used to determine the relative contributions of PHI and its C‐terminally extended forms, peptide histidine glycine (PHI‐Gly) and peptide histidine valine [PHV(1–42)], to the PHI‐LI released by the rat gastric fundus. 3 In the presence of atropine (1 μ m ) and guanethidine (5 μ m ), EFS (120 mA, 1ms, 0.25–32.0 Hz, trains of 2 min) induced frequency‐dependent relaxations of 5‐hydroxytryptamine (3 μ m ) pre‐contracted strips. 4 EFS at frequencies of 8–32 Hz evoked significant increases in PHI‐LI outflow. The increases in PHI‐LI outflow evoked by 16‐Hz EFS were abolished by tetrodotoxin (3 μ m ) and by a calcium‐free medium, indicating an active release process from intramural nerves. 5 The EFS‐induced release of PHI‐LI measured with the N‐terminal‐specific antiserum was significantly greater than that detected with the C‐terminal‐specific antisera. 6 Sephadex G‐25 gel permeation chromatographic analysis was performed on the PHI‐LI released in response to 32‐Hz EFS. A C‐terminal‐specific antiserum revealed one peak co‐eluting with the rat PHI standard. When PHI‐LI was measured with the N‐terminal‐specific antiserum, two peaks were found that co‐eluted with the rat PHV(1–42) and rat PHI‐Gly/PHI standards, respectively. 7 The present data suggest that the extended forms of PHI are the primary components of the PHI‐LI released by NANC inhibitory neurones in the rat gastric fundus and support a NANC inhibitory neurotransmitter role for PHI and its extended forms in this tissue.