JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Catravas, J. D.
Right arrow Articles by El Kashef, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Catravas, J. D.
Right arrow Articles by El Kashef, H.

Effects of acetylcholine in the pulmonary circulation of rabbits

JD Catravas, JJ Buccafusco and H El Kashef

The pulmonary and systemic vascular beds differ in their response to several vasoactive substances. Acetylcholine (ACh) is a potent systemic vasodilator; however, its effects on the pulmonary circulation are not clear. Utilizing the isolated rabbit lung preparation perfused in situ under constant flow (92 +/- 3 ml/min) with an albumin-enriched physiologic salt solution, we studied the effects of graded concentrations of ACh (10(-10) to 10(-4) M) in the recirculating perfusate on pulmonary arterial pressure (PAP). The lungs were ventilated to 15 cm of water with 97% O2-3% CO2. ACh (10(-8) to 4 X 10(- 7) M) produced a dose-dependent increase in PAP which required up to 20 min to return to predrug levels. Physostigmine (10(-5) M) maintained the maximal PAP response to ACh for the duration of the experiment (up to 2 hr). Higher concentrations of ACh produced rapid increases in PAP resulting in edema. Pre- or post-treatment with the muscarinic receptor antagonist atropine (10(-5) M) completely prevented or reversed the pressor effects of ACh, respectively. Histamine receptor (H1 and H2) or angiotensin II receptor blockade had no effect on the PAP actions of ACh, however pretreatment with the prostaglandin synthesis (cyclooxygenase) inhibitor indomethacin (10(-5) M) or aspirin (10(-3) M), completely abolished the PAP response to ACh up to concentrations of 10(-4) M. In experiments in which airway pressure was allowed to vary, it rose significantly in response to increasing concentrations of ACh. ACh-induced increases in airway pressure were unaffected by pretreatment with indomethacin (10(-5) M) but were totally inhibited by pretreatment with atropine (10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Volume 231, Issue 2, pp. 236-241, 11/01/1984
Copyright © 1984 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
T. Ogasa, H. Nakano, H. Ide, Y. Yamamoto, N. Sasaki, S. Osanai, Y. Akiba, K. Kikuchi, and J. Iwamoto
Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs
J Appl Physiol, July 1, 2001; 91(1): 363 - 370.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. C. O'Donnell, M. L. Tod, and J. B. Gordon
Developmental changes in endothelium-dependent relaxation of pulmonary arteries: role of EDNO and prostanoids
J Appl Physiol, November 1, 1996; 81(5): 2013 - 2019.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1984 by the American Society for Pharmacology and Experimental Therapeutics.