NO modulation of myocardial performance in fish hearts

Tota, Bruno; Amelio, Daniela; Pellegrino, Daniela; Ip, Yuen K.; Cerra, Maria Carmela

doi:10.1016/j.cbpb.2005.04.019

Cited by 73 publications

(42 citation statements)

References 57 publications

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“…cGMP/PKG activation is considered a major transduction pathway for NO cardiac regulation, whereby, among other effects, it induces myofilament desensitization to Ca 2þ , thought to be responsible for accelerated myocardial relaxation through troponin I phosphorylation at Ser23/24 (Layland et al 2002). In the working eel heart, the NO-induced cGMP-PKG pathway remarkably modulates mechanical performance (see, for references, Tota et al 2005). For example, it tonically decreases SV either under basal condition (Imbrogno et al 2001) or following endoluminal chemical stimulations of AT 1 angiotensin II receptors (Imbrogno et al 2003), or b 3 adrenergic receptors (Imbrogno et al 2006), or exposure to the anti-adrenergic cardio-inhibitory peptide vasostatin I (Imbrogno et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Phospholamban S-nitrosylation modulates Starling response in fish heart

et al. 2009

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The Frank -Starling mechanism is a fundamental property of the vertebrate heart, which allows the myocardium to respond to increased filling pressure with a more vigorous contraction of its lengthened fibres. In mammals, myocardial stretch increases cardiac nitric oxide (NO) release from both vascular endothelium and cardiomyocytes. This facilitates myocardial relaxation and ventricular diastolic distensibility, thus influencing the Frank -Starling mechanism.In the in vitro working heart of the eel Anguilla anguilla, we previously showed that an endogenous NO release affects the Frank -Starling response making the heart more sensitive to preload. Using the same bioassay, we now demonstrate that this effect is confirmed in the presence of the exogenous NO donor S-nitroso-N-acetyl penicillamine, is independent from endocardial endothelium and guanylate cyclase/ cGMP/protein kinase G and cAMP/protein kinase A pathways, involves a PI(3)kinase-mediated activation of endothelial NO synthase and a modulation of the SR-CA 2þ ATPase (SERCA2a) pumps. Furthermore, we show that NO influences cardiac response to preload through S-nitrosylation of phospholamban and consequent activation of SERCA2a. This suggests that in the fish heart NO modulates the Frank -Starling response through a beat-to-beat regulation of calcium reuptake and thus of myocardial relaxation.We propose that this mechanism represents an important evolutionary step for the stretch-induced intrinsic regulation of the vertebrate heart, providing, at the same time, a stimulus for mammalian-oriented studies.

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Section: Discussionmentioning

confidence: 99%

Phospholamban S-nitrosylation modulates Starling response in fish heart

et al. 2009

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“…In fish, significant NOS expression has been reported in brain, heart and gills (Brüning et al, 1995;Holmqvist et al, 2000;Tota et al, 2005;Ebbesson et al, 2005;Hyndman et al, 2006), the tissues with the highest nitrite levels in goldfish. The values of [SNO] and [FeNO + NNO] in tissues range from practically zero (below detection level) in the gills (Fig.8C) to values that are comparable with nitrite concentrations in kidney and liver (Fig.7), which points to significant differences in the extent and importance of nitros(yl)ation reactions among tissues.…”

Section: Basal Normoxic Values Of No Metabolitesmentioning

confidence: 99%

“…Teleost fish express NOS enzymes, and albeit conflicting results are available in the literature, it appears that the functional roles of NO in teleost fish and mammals are comparable (Tota et al, 2005;Agnisola, 2005;Pelster, 2007;Olson and Donald, 2009). Similarly, nitrite may function as a NO donor under hypoxic conditions in fish, and the importance could exceed that in mammals, given that many fish species naturally experience fluctuating or chronic low ambient P O2 values (Jensen, 2009a).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide metabolites in goldfish under normoxic and hypoxic conditions

Hansen

Frank

2010

Journal of Experimental Biology

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SUMMARYNitric oxide (NO), produced by nitric oxide synthases (NOS enzymes), regulates multiple physiological functions in animals. NO exerts its effects by binding to iron (Fe) of heme groups (exemplified by the activation of soluble guanylyl cyclase) and by Snitrosylation of proteins -and it is metabolized to nitrite and nitrate. Nitrite is used as a marker for NOS activity but it is also a NO donor that can be activated by various cellular proteins under hypoxic conditions. Here, we report the first systematic study of NO metabolites (nitrite, nitrate, S-nitroso, N-nitroso and Fe-nitrosyl compounds) in multiple tissues of a non-mammalian vertebrate (goldfish) under normoxic and hypoxic conditions. NO metabolites were measured in blood (plasma and red cells) and heart, brain, gill, liver, kidney and skeletal muscle, using highly sensitive reductive chemiluminescence. The severity of the chosen hypoxia levels was assessed from metabolic and respiratory variables. In normoxic goldfish, the concentrations of NO metabolites in plasma and tissues were comparable with values reported in mammals, indicative of similar NOS activity. Exposure to hypoxia [at P O2 (partial pressure of O 2 ) values close to and below the critical P O2 ] for two days caused large decreases in plasma nitrite and nitrate, which suggests reduced NOS activity and increased nitrite/nitrate utilization or loss. Tissue NO metabolites were largely maintained at their tissue-specific values under hypoxia, pointing at nitrite transfer from extracellular to intracellular compartments and cellular NO generation from nitrite. The data highlights the preference of goldfish to defend intracellular NO homeostasis during hypoxia.

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“…In vertebrates, NO controls a vast array of metabolic and systemic responses, including vasodilatation and cellular metabolic activities (Moncada et al, 1991), particularly within the heart (Tota et al, 2005;Gödecke, 2006;Flögel et al, 2010). These responses involve two major specific targets of NO, namely soluble guanylate cyclase in the vasculature, and cytochrome c oxidase (complex IV) in the mitochondria (Hill et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Circulating nitric oxide metabolites and cardiovascular changes in the turtleTrachemys scriptaduring normoxia, anoxia and reoxygenation

Jacobsen

Hansen

Frank

et al. 2012

Journal of Experimental Biology

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SUMMARYTurtles of the genus Trachemys show a remarkable ability to survive prolonged anoxia. This is achieved by a strong metabolic depression, redistribution of blood flow and high levels of antioxidant defence. To understand whether nitric oxide (NO), a major regulator of vasodilatation and oxygen consumption, may be involved in the adaptive response of Trachemys to anoxia, we measured NO metabolites (nitrite, S-nitroso, Fe-nitrosyl and N-nitroso compounds) in the plasma and red blood cells of venous and arterial blood of Trachemys scripta turtles during normoxia and after anoxia (3h) and reoxygenation (30min) at 21°C, while monitoring blood oxygen content and circulatory parameters. Anoxia caused complete blood oxygen depletion, decrease in heart rate and arterial pressure, and increase in venous pressure, which may enhance heart filling and improve cardiac contractility. Nitrite was present at high, micromolar levels in normoxic blood, as in some other anoxia-tolerant species, without significant arterial-venous differences. Normoxic levels of erythrocyte S-nitroso compounds were within the range found for other vertebrates, despite very high measured thiol content. Fe-nitrosyl and N-nitroso compounds were present at high micromolar levels under normoxia and increased further after anoxia and reoxygenation, suggesting NO generation from nitrite catalysed by deoxygenated haemoglobin, which in turtle had a higher nitrite reductase activity than in hypoxia-intolerant species. Taken together, these data indicate constitutively high circulating levels of NO metabolites and significant increases in blood NO after anoxia and reoxygenation that may contribute to the complex physiological response in the extreme anoxia tolerance of Trachemys turtles.

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NO modulation of myocardial performance in fish hearts

Cited by 73 publications

References 57 publications

Phospholamban S-nitrosylation modulates Starling response in fish heart

Phospholamban S-nitrosylation modulates Starling response in fish heart

Nitric oxide metabolites in goldfish under normoxic and hypoxic conditions

Circulating nitric oxide metabolites and cardiovascular changes in the turtleTrachemys scriptaduring normoxia, anoxia and reoxygenation

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