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Increased intracellular levels of calcitonin gene‐related peptide‐like immunoreactivity in pulmonary endocrine cells of hypoxic rats
Author(s) -
Springall D. R.,
Collina G.,
Barer G.,
Suggett A. J.,
Bee D.,
Polak J. M.
Publication year - 1988
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711550312
Subject(s) - calcitonin gene related peptide , enteroendocrine cell , medicine , endocrinology , calcitonin , immunostaining , endocrine system , biology , hypoxia (environmental) , peptide hormone , hormone , neuropeptide , chemistry , receptor , immunohistochemistry , organic chemistry , oxygen
Abstract The mammalian respiratory tract contains innervated groups of endocrine cells which are believed to respond to hypoxia. We have demonstrated the involvement of a specific regulatory peptide produced by the cells, calcitonin generelated peptide (CGRP), in this response. Cells immunoreactive for CGRP or for protein gene product 9·5 (PGP 9·5), a general marker of nerves and endocrine cells, were quantified in sections of lungs from hypoxic (21 days, 10 percent 0 2 ) and normoxic rats. An immunostaining method employing supra‐optimal dilutions of primary antiserum was used. This detects variations in antigen concentration which may be masked if the routine, optimal dilution is used. The number of CGRP‐immunoreactive endocrine cells was significantly ( P < 0·001) greater in the lungs of hypoxic rats (76·9 ± 10·1 cells/cm 2 , mean ± SEM) compared with controls (19·7 ± 2·4). However, the numbers of PGP 9·5‐immunoreactive cells were the same in both groups (81·3 ± 12·2, hypoxic; 79·5 ± 9·8 control), suggesting that the total number of endocrine cells did not change. It is concluded therefore that the apparent increase in CGRP‐immunoreactive endocrine cells in hypoxic rat lungs is due to increased intracellular levels of the peptide. Since CGRP is a vasodilator, this could have important implications in the vasoconstrictor response to hypoxia.