Co-occurrence of immunoreactive calcitonin and calcitonin gene-related peptide in neuroendocrine cells of rat lungs

1991 ◽  
Vol 264 (3) ◽  
pp. 555-561 ◽  
Author(s):  
Tooru Shimosegawa ◽  
Sami I. Said
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Neuroendocrine Cells ◽  
Related Peptide ◽  
Rat Lungs ◽  
Calcitonin Gene

Calcitonin gene-related peptide and its mRNA in pulmonary neuroendocrine cells and ganglia

1991 ◽  
Vol 96 (4) ◽  
pp. 311-315 ◽  
Author(s):  
I. M. Keith ◽  
M. Pelto-Huikko ◽  
M. Schalling ◽  
T. H�kfelt
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Neuroendocrine Cells ◽  
Related Peptide ◽  
Pulmonary Neuroendocrine Cells ◽  
Calcitonin Gene

Proximal airway mucous cells of ovalbumin-sensitized and -challenged Brown Norway rats accumulate the neuropeptide calcitonin gene-related peptide

2004 ◽  
Vol 287 (2) ◽  
pp. L286-L295 ◽  
Author(s):  
Shawnessy D. Larson ◽  
Charles G. Plopper ◽  
Greg Baker ◽  
Brian K. Tarkington ◽  
Kendra C. Decile ◽  
...  
Keyword(s):  
Periodic Acid ◽  
Mucous Cell ◽  
Calcitonin Gene Related Peptide ◽  
Neuroendocrine Cells ◽  
Brown Norway ◽  
Mucous Cells ◽  
Periodic Acid Schiff ◽  
Related Peptide ◽  
Afferent Nerves ◽  
Calcitonin Gene

Mucous cell hypersecretion and increased neuropeptide production play a role in the exacerbation of symptoms associated with asthma. The source of these neuropeptides have been confined to the contributions of small afferent nerves or possibly neuroendocrine cells. We tested the hypothesis that repeated exposure to allergen would alter the sources and abundance of neuropeptides in airways. Right middle lobes from rats (8 wk old) exposed to 2.5% ovalbumin (OVA) for five episodes (30 min each) or filtered air were inflation fixed with paraformaldehyde. The lobes were dissected to expose the airway tree, permeabilized with DMSO, and incubated in antibody to rat calcitonin gene-related peptide (CGRP), followed with a fluorochrome-labeled second antibody. CGRP-positive structures were imaged via confocal microscopy. Airways were later embedded in plastic and sectioned for cell identification. In animals challenged with OVA, CGRP-positive cells, not neuroendocrine or neuronal in origin (confirmed by a lack of protein gene product 9.5 signal), were recorded along the axial path. In section, this fluorescent signal was localized to granules within epithelial cells. Alcian blue/periodic acid-Schiff staining of these same sections positively identify these cells as mucous cells. Mucous cells of animals not challenged with OVA were not positive for CGRP. We conclude that episodic allergen exposure results in the accumulation of CGRP within mucous cells, creating a new source for the release of this neuropeptide within the airway.

Calcitonin gene-related peptide modulates pulmonary vascular reactivity in isolated rat lungs

1994 ◽  
Vol 77 (1) ◽  
pp. 142-146 ◽  
Author(s):  
P. L. Janssen ◽  
A. Tucker
Keyword(s):  
Vascular Reactivity ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Calcitonin Gene Related Peptide ◽  
Ang Ii ◽  
Related Peptide ◽  
Pulmonary Vasoconstriction ◽  
Rat Lungs ◽  
Pressor Responses ◽  
Calcitonin Gene

The role of calcitonin gene-related peptide (CGRP) in modulating hypoxic pulmonary vasoconstriction was assessed. The effects of CGRP and its antagonist [CGRP-(8–37)] on responses to acute hypoxia (3% O2) and angiotensin II (ANG II; 0.4 microgram) were studied in isolated lungs of male Sprague-Dawley rats perfused with a salt solution. Rats with pulmonary hypertension, induced by simulated altitude exposure, were also used to determine the actions of CGRP in a remodeled pulmonary vascular bed. In normotensive (NT) and altitude-exposed (AE) lungs, CGRP injections (10 nM), given after stable pressor responses were attained, attenuated (P < 0.05) subsequent hypoxic pressor responses. Pretreatment with CGRP-(8–37) (10 nM) enhanced (P < or = 0.05) initial ANG II-induced pressor responses in both AE and NT lungs. CGRP-(8–37) pretreatment (10 nM) had little influence on the hypoxic pressor responses in either NT or AE lungs. Results indicate that CGRP modulates hypoxic pulmonary vasoconstriction and that CGRP-(8–37) enhances pressor responses to ANG II in NT and AE rat lungs.

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