| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Dipartimento di Scienze Cliniche e Biologiche and 2 Dipartimento di Neuroscienze, Sezione di Fisiologia, dell'Università di Torino, 10043 Orbassano (TO), Italy; and 3 Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-6568
This study focused on the mechanisms of the negative inotropic response to bradykinin (BK) in isolated rat hearts perfused at constant flow. BK (100 nM) significantly reduced developed left ventricular pressure (LVP) and the maximal derivative of systolic LVP by 20-22%. The cytochrome P-450 (CYP) inhibitors 1-aminobenzotriazole (1 mM and 100 µM) or proadifen (5 µM) abolished the cardiodepression by BK, which was not affected by nitric oxide and cyclooxygenase inhibitors (35 µM NG-nitro-L-arginine methyl ester and 10 µM indomethacin, respectively). The CYP metabolite 14,15-epoxyeicosatrienoic acid (14,15-EET; 50 ng/ml) produced effects similar to those of BK in terms of the reduction in contractility. After the coronary endothelium was made dysfunctional by Triton X-100 (0.5 µl), the BK-induced negative inotropic effect was completely abolished, whereas the 14,15-EET-induced cardiodepression was not affected. In hearts with normal endothelium, after recovery from 14,15-EET effects, BK reduced developed LVP to a 35% greater extent than BK in the control. In conclusion, CYP inhibition or endothelial dysfunction prevents BK from causing cardiodepression, suggesting that, in the rat heart, endothelial CYP products mediate the negative inotropic effect of BK. One of these mediators appears to be 14,15-EET.
endothelium; epoxyeicosatrienoic acids; myocardial contractility; left ventricular pressure; coronary perfusion pressure
This article has been cited by other articles:
|
|
 |
|
  S. Cappello, T. Angelone, B. Tota, P. Pagliaro, C. Penna, R. Rastaldo, A. Corti, G. Losano, and M. C. Cerra Human recombinant chromogranin A-derived vasostatin-1 mimics preconditioning via an adenosine/nitric oxide signaling mechanism Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H719 - H727. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Penna, D. Mancardi, R. Rastaldo, G. Losano, and P. Pagliaro Intermittent activation of bradykinin B2 receptors and mitochondrial KATP channels trigger cardiac postconditioning through redox signaling Cardiovasc Res, July 1, 2007; 75(1): 168 - 177. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Penna, G. Alloatti, S. Cappello, D. Gattullo, G. Berta, B. Mognetti, G. Losano, and P. Pagliaro Platelet-activating factor induces cardioprotection in isolated rat heart akin to ischemic preconditioning: role of phosphoinositide 3-kinase and protein kinase C activation Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2512 - H2520. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Ohta, N. Hasebe, S. Tsuji, K. Izawa, Y.-T. Jin, S. Kido, S. Natori, M. Sato, and K. Kikuchi Unequal effects of renin-angiotensin system inhibitors in acute cardiac dysfunction induced by isoproterenol Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2914 - H2921. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Seubert, B. Yang, J. A. Bradbury, J. Graves, L. M. Degraff, S. Gabel, R. Gooch, J. Foley, J. Newman, L. Mao, et al. Enhanced Postischemic Functional Recovery in CYP2J2 Transgenic Hearts Involves Mitochondrial ATP-Sensitive K+ Channels and p42/p44 MAPK Pathway Circ. Res., September 3, 2004; 95(5): 506 - 514. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Kreutzer and T. Jue Role of myoglobin as a scavenger of cellular NO in myocardium Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H985 - H991. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
