![]() |
|
|
Vol. 300, Issue 1, 324-329, January 2002
Birmingham Veteran Affairs Medical Center, Department of Medicine,
Hypertension and Vascular Biology Program, Division of Cardiovascular
Disease, and Department of Physiology and Biophysics, University
of Alabama, Birmingham, Alabama (C-C.W., D.M.F., W.E.B., L.J.D.);
Hypertension/Vascular Disease Center, Wake Forest University School of
Medicine, Winston-Salem, North Carolina (C.M.F., K.B.B.); and
Department of Medicine, Medical University of South Carolina,
Charleston, South Carolina (A.A.J.)
We previously demonstrated the substantial capacity for angiotensin
(ANG) II formation in the interstitium of the dog heart in vivo. The
current study tested the hypothesis that interstitial fluid (ISF)
bradykinin (BK) is influenced by ANG II formation. Four microdialysis
probes were inserted into the left ventricular myocardium of
eight open-chest anesthetized dogs. The probe effluent was collected
during four stages in each dog. Probes 1 and 3 sequentially delivered:
1) buffer; 2) ANG I (15 µM); 3) ANG II type 1 receptor antagonist
(AT1-ant; irbesartan, 50 µM) or AT2-ant
(PD123319, 50 µM); and 4) ANG I + AT1-ant or ANG I + AT2-ant. Probes 2 and 4 used the same protocol,
substituting ANG II for ANG I in a concentration (0.5 µM) equivalent
to that achieved during ANG I infusion. ISF BK levels increased 15-fold
during ANG I (p < 0.001) but not during ANG II
infusion. Co-infusion of selective AT1- and
AT2-ants or nonselective AT-ant did not block the increase
in ISF BK. ISF infusions of ANG I also produced a greater than 400-fold
rise in ISF ANG-(1-7) over baseline. ISF infusion of ANG-(1-7) (10 µM) produced a 15-fold increase in ISF BK (p < 0.001). The metabolic machinery exists for the formation of BK and
ANG-(1-7) in the cardiac ISF space that is not blocked by an AT
receptor antagonist. The differential increase in ISF BK during ANG I
and ANG-(1-7) but not during ANG II infusions suggests the possibility
of decreased catabolism of ISF BK by an angiotensin-converting enzyme
due to active site occupation by ANG I and ANG-(1-7).
This article has been cited by other articles:
![]() |
P. J. Garabelli, J. G. Modrall, J. M. Penninger, C. M. Ferrario, and M. C. Chappell Distinct roles for angiotensin-converting enzyme 2 and carboxypeptidase A in the processing of angiotensins within the murine heart Exp Physiol, May 1, 2008; 93(5): 613 - 621. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Ferrario, A. J. Trask, and J. A. Jessup Advances in biochemical and functional roles of angiotensin-converting enzyme 2 and angiotensin-(1-7) in regulation of cardiovascular function Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2281 - H2290. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. A. Tallant, C. M. Ferrario, and P. E. Gallagher Angiotensin-(1-7) inhibits growth of cardiac myocytes through activation of the mas receptor Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1560 - H1566. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. M. Multani, J. S. Ikonomidis, P. Y. Kim, E. A. Miller, K. J. Payne, R. Mukherjee, B. H. Dorman, and F. G. Spinale Dynamic and differential changes in myocardial and plasma endothelin in patients undergoing cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., March 1, 2005; 129(3): 584 - 590. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Ishiyama, P. E. Gallagher, D. B. Averill, E. A. Tallant, K. B. Brosnihan, and C. M. Ferrario Upregulation of Angiotensin-Converting Enzyme 2 After Myocardial Infarction by Blockade of Angiotensin II Receptors Hypertension, May 1, 2004; 43(5): 970 - 976. [Abstract] [Full Text] [PDF] |
||||
![]() |
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] |
||||
![]() |
D. B. Averill, Y. Ishiyama, M. C. Chappell, and C. M. Ferrario Cardiac Angiotensin-(1-7) in Ischemic Cardiomyopathy Circulation, October 28, 2003; 108(17): 2141 - 2146. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Nishiyama, D. M. Seth, and L. G. Navar Renal Interstitial Fluid Angiotensin I and Angiotensin II Concentrations during Local Angiotensin-Converting Enzyme Inhibition J. Am. Soc. Nephrol., September 1, 2002; 13(9): 2207 - 2212. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Ferrario Does Angiotensin-(1-7) Contribute to Cardiac Adaptation and Preservation of Endothelial Function in Heart Failure? Circulation, April 2, 2002; 105(13): 1523 - 1525. [Full Text] [PDF] |
||||