AJP - Regu AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 274: R120-R125, 1998;
0363-6119/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Sakakibara, T.
Right arrow Articles by Nasjletti, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sakakibara, T.
Right arrow Articles by Nasjletti, A.
Vol. 274, Issue 1, R120-R125, January 1998

Determinants of kinin release in isolated rat hindquarters

Tohru Sakakibara, Thomas H. Hintze, and Alberto Nasjletti

Departments of Physiology and Pharmacology, New York Medical College, Valhalla, New York 10595

We studied the determinants of kinin release into the venous effluent of rat hindquarters perfused with Krebs bicarbonate buffer. Kinin release in preparations perfused with control media (14.6 ± 2.5-20.7 ± 6.7 pg/15 min) was surpassed by that in preparations perfused with media containing kininase inhibitors (243 ± 53 to 276 ± 78 pg/15 min). Kinin release increased when purified kininogen (from 242 ± 43 to 3,365 ± 725 pg/15 min) or kallikrein (from 270 ± 49 to 30,649 ± 8,040 pg/15 min) was added to the perfusate. Conversely, kinin release fell when the kallikrein inhibitor aprotinin (from 272 ± 58 to 122 ± 27 pg/15 min) or soybean trypsin inhibitor (from 273 ± 52 to 195 ± 25 pg/15 min) was added. Both basal and kininogen-induced kinin release were attenuated in preparations perfused with media containing cycloheximide, a protein synthesis inhibitor, but kallikrein-induced kinin release was not. These data suggest that kinin release from perfused rat hindquarters reflects the activity of both the kinin-degrading and kinin-generating pathways and that the latter is sustained by a kallikrein manufactured de novo and by preexistent kininogen(s).

plasma kallikrein; vascular kallikrein; kininogens; kininases; bradykinin


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Tan, F. N. Hutchison, and A. A. Jaffa
Mechanisms of angiotensin II-induced expression of B2 kinin receptors
Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H926 - H932.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
C. L. Dumke, J. Kim, E. B. Arias, and G. D. Cartee
Role of kallikrein-kininogen system in insulin-stimulated glucose transport after muscle contractions
J Appl Physiol, February 1, 2002; 92(2): 657 - 664.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
P. S. Naidu, V. Velarde, C. S. Kappler, R. C. Young, R. K. Mayfield, and A. A. Jaffa
Calcium-calmodulin mediates bradykinin-induced MAPK phosphorylation and c-fos induction in vascular cells
Am J Physiol Heart Circ Physiol, September 1, 1999; 277(3): H1061 - H1068.
[Abstract] [Full Text] [PDF]


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