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


     

J Appl Physiol 76: 1439-1444, 1994;
8750-7587/94 $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 Tamaoki, J.
Right arrow Articles by Konno, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tamaoki, J.
Right arrow Articles by Konno, K.

Journal of Applied Physiology, Vol 76, Issue 4 1439-1444, Copyright © 1994 by American Physiological Society

ARTICLES

Angiotensin II 1 receptor-mediated contraction of pulmonary artery and its modulation by prolylcarboxypeptidase

J. Tamaoki, F. Sugimoto, E. Tagaya, K. Isono, A. Chiyotani and K. Konno
First Department of Medicine, Tokyo Women's Medical College, Japan.

To determine the subtype of angiotensin II (ANG II) receptor involved in the contraction of pulmonary artery and to elucidate its possible modulation by endogenous peptidases, we studied canine isolated pulmonary arterial rings under isometric conditions in vitro. Addition of ANG II caused a concentration-dependent contraction, an effect that was not altered by the ANG II 2 receptor antagonist EXP655 but was depressed by the ANG II 1 receptor antagonist DuP 753 so that the ANG II response curves were displaced to higher concentration by 1.5-2.0 log U (P < 0.001). Pretreatment of tissues with the prolylcarboxypeptidase (PCP) inhibitor p-methylphenyl sulfonyl-fluoride potentiated the ANG II-induced contraction, with the concentration required to produce a half-maximal effect of ANG II being decreased from 4.1 +/- 0.9 x 10(-9) to 3.8 +/- 0.5 x 10(-10) M (P < 0.001), whereas other peptidase inhibitors such as p-chloromercuriphenyl sulfonic acid, amastatin, and phosphoramidon had no effect. The p-methylphenyl sulfonylfluoride-induced potentiation was abolished by the removal of endothelium, but it was still observed in the presence of NG-nitro-L-arginine methyl ester in the endothelium-intact tissues. The PCP activity in the tissues was reduced by the removal of endothelium from 645 +/- 88 to 91 +/- 29 nmol.mg protein-1.h-1 (P < 0.001), and cultured endothelium had the activity of 404 +/- 39 nmol.mg protein-1.h-1. These results suggest that ANG II contracts pulmonary artery via ANG II 1 receptor and that PCP localized to the endothelium may have a modulatory role in the ANG II-induced pulmonary vasoconstriction.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
M. O. Krebs, W. Boemke, S. Simon, M. Wenz, and G. Kaczmarczyk
Acute hypoxic pulmonary vasoconstriction in conscious dogs decreases renin and is unaffected by losartan
J Appl Physiol, June 1, 1999; 86(6): 1914 - 1919.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
C. L. Ivey, B. J. Roy, and M. I. Townsley
Ablation of lung endothelial injury after pacing-induced heart failure is related to alterations in Ca2+ signaling
Am J Physiol Heart Circ Physiol, September 1, 1998; 275(3): H844 - H851.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. S. Damron, H. S. Nadim, S. J. Hong, A. Darvish, and P. A. Murray
Intracellular translocation of PKC isoforms in canine pulmonary artery smooth muscle cells by ANG II
Am J Physiol Lung Cell Mol Physiol, February 1, 1998; 274(2): L278 - L288.
[Abstract] [Full Text] [PDF]


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