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Journal of Experimental Biology, Vol 204, Issue 10 1719-1727, Copyright © 2001 by Company of Biologists
JOURNAL ARTICLES |
S Imbrogno, L De Iuri, R Mazza and B Tota
Department of Cell Biology, University of Calabria, Italy and Zoological Station 'A. Dohrn', Villa Comunale, I-80121 Naples, Italy. tota@unical.it
Nothing is known about the effects of nitric oxide (NO) on cardiac performance in fish. Using an in vitro working heart preparation that generates physiological values of output pressure, cardiac output and ventricular work and power, we assessed the effects of NO on the cardiac performance of the eel Anguilla anguilla. We examined basal cardiac performance (at constant preload, afterload and heart rate), the effects of cholinergic stimulation and the Frank-Starling response (preload-induced increases in cardiac output at constant afterload and heart rate). The NO synthase (NOS) inhibitors N(G)-monomethyl-l-arginine (l-NMMA) and l-N(5)(1-iminoethyl)ornithine (l-NIO), the guanylate cyclase inhibitor 1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ) and Triton X-100, a detergent that damages the endocardial endothelium, all increased stroke volume (V(S)) and stroke work (W(S)). In contrast, the endogenous NOS substrate l-arginine, tested before and after treatment with haemoglobin, the NO donor 3-morpholinosydnonimine, tested with and without the superoxide scavenger superoxide dismutase, and the stable cGMP analogue 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP) decreased V(S) and W(S). Acetylcholine chloride produced a biphasic effect. At nanomolar concentrations, in 34 % of the preparations, it induced a NO-cGMP-dependent positive inotropism that required the integrity of the endocardial endothelium. Pretreatment with Triton X-100 or with NO-cGMP pathway inhibitors (l-NMMA, l-NIO, N(G)-nitro-l-arginine methyl ester, Methylene Blue and ODQ) abolished the positive effect of acetylcholine. In contrast, at micromolar concentrations, acetylcholine produced a negative effect that involved neither the endocardial endothelium nor the NO-cGMP pathway. Pre-treatment with l-arginine (10(-)(6 )mol l(-)(1)) was without effect, whereas l-NIO (10(-)(5 )mol l(-)(1)) significantly reduced the Frank-Starling response. Taken together, these three experimental approaches provide evidence that NO modulates cardiac performance in the eel heart.
This article has been cited by other articles:
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  S. Imbrogno, T. Angelone, C. Adamo, E. Pulera, B. Tota, and M. C. Cerra Beta3-Adrenoceptor in the eel (Anguilla anguilla) heart: negative inotropy and NO-cGMP-dependent mechanism J. Exp. Biol., December 15, 2006; 209(24): 4966 - 4973. [Abstract] [Full Text] [PDF]
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D. Pellegrino, C. A. Palmerini, and B. Tota No hemoglobin but NO: the icefish (Chionodraco hamatus) heart as a paradigm J. Exp. Biol., October 15, 2004; 207(22): 3855 - 3864. [Abstract] [Full Text] [PDF]
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M. C. Cerra, S. Imbrogno, D. Amelio, F. Garofalo, E. Colvee, B. Tota, and J. M. Icardo Cardiac morphodynamic remodelling in the growing eel (Anguilla anguilla L.) J. Exp. Biol., July 15, 2004; 207(16): 2867 - 2875. [Abstract] [Full Text] [PDF]
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R. S. Farrar and K. J. Rodnick Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout J. Exp. Biol., May 15, 2004; 207(12): 2083 - 2093. [Abstract] [Full Text] [PDF]
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J. S. Cameron, K. E. Hoffmann, C. Zia, H. M. Hemmett, A. Kronsteiner, and C. M. Lee A role for nitric oxide in hypoxia-induced activation of cardiac KATP channels in goldfish (Carassius auratus) J. Exp. Biol., November 15, 2003; 206(22): 4057 - 4065. [Abstract] [Full Text] [PDF]
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S. Imbrogno, M. C. Cerra, and B. Tota Angiotensin II-induced inotropism requires an endocardial endothelium-nitric oxide mechanism in the in-vitro heart of Anguilla anguilla J. Exp. Biol., August 1, 2003; 206(15): 2675 - 2684. [Abstract] [Full Text] [PDF]
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