Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 58: 1291-1297, 1985;
8750-7587/85 $5.00
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 Email this article to a friend
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 Tanaka, D. T.
Right arrow Articles by Grunstein, M. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tanaka, D. T.
Right arrow Articles by Grunstein, M. M.

Journal of Applied Physiology, Vol 58, Issue 4 1291-1297, Copyright © 1985 by American Physiological Society


ARTICLES

Vasoactive effects of substance P on isolated rabbit pulmonary artery

D. T. Tanaka and M. M. Grunstein

The vasoactive properties of substance P (SP) were studied in isolated rabbit pulmonary artery (PA) segments in vitro. In the absence of active base-line tone, noncumulative administration of SP (10(-11) to 10(-4) M) produced dose-dependent increases in PA tension. The peak isometric tension (Tmax) with SP was similar to the Tmax response to epinephrine; however, the doses of the agonist producing a threshold contraction and 25% of Tmax (ED25) were significantly lower for SP. In the presence of active base-line tone, induced by epinephrine or 5-hydroxytryptamine, SP produced transient PA relaxation which was directly related to the magnitude of the precontracted PA tension. Blockade of neurotransmission with tetrodotoxin (1 microgram/ml) and antagonists to alpha 1-adrenergic and histamine receptor binding had no effect on the contractile response to SP. On the other hand, PA contraction to an ED50 dose of SP was 1) inhibited by a mean of 33 +/- 10% (SE) following pretreatment with the cholinesterase inhibitor, neostigmine (10(-6) M) and 2) augmented by 52 +/- 21% with the cholinergic antagonist, atropine (10(-4) M). The latter also completely blocked the relaxation response to SP in precontracted PA. Similarly, removal of the PA endothelium also abolished the relaxation response to SP. In contrast, SP-induced contraction was markedly inhibited by the cyclooxygenase inhibitor, meclofenamate (1 microgram/ml), as well as the SP antagonist, D-Pro2, D-Trp7,9-SP.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
Y.-L. Lai, S.-J. Chu, M.-C. Ma, and C.-F. Chen
Temporal increase in the reactivity of pulmonary vasculature to substance P in chronically hypoxic rats
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2002; 282(3): R858 - R864.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
P.J. Boels, J. Deutsch, B. Gao, and S.G. Haworth
Maturation of the response to bradykinin in resistance and conduit pulmonary arteries
Cardiovasc Res, November 1, 1999; 44(2): 416 - 428.
[Abstract] [Full Text] [PDF]


Home page
Toxicol Ind HealthHome page
W. J. Meggs
Mechanisms of allergy and chemical sensitivity
Toxicology and Industrial Health, April 1, 1999; 15(3-4): 331 - 338.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online