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Comment
. 2004 Nov 23;101(47):16403-4.
doi: 10.1073/pnas.0405859101. Epub 2004 Nov 16.

NO and superoxide: opposite ends of the seesaw in cardiac contractility

Joseph Bonaventura  1 , Andrew Gow
Affiliations
Comment

NO and superoxide: opposite ends of the seesaw in cardiac contractility

Joseph Bonaventura et al. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Fig. 1.
Fig. 1.
nNOS and XOR are expressed within close proximity within the SR. nNOS catalyzes the conversion of arginine to citruline with the concomitant production of the NO group. NO produced in this way is capable of nitrosylating a specific cysteine on the SR calcium channel, otherwise called RyR (19). SNO formation on the RyR increases channel opening probability and hence calcium release during excitation–contraction coupling. XOR, in the oxidase form, utilizes molecular oxygen as an electron acceptor for purine metabolism to produce superoxide (formula image). Superoxide is capable of diffusing out of the SR and inhibiting the calcium responsiveness of the contractile machinery, thus inhibiting contraction (6, 20). In addition to activating calcium release through the RyR, NO can increase contractility by inhibiting the release of superoxide from the SR by direct reaction (solid red arrow). Additionally, superoxide may be able to inhibit contractility by inhibiting NO-mediated activation of the RyR (dashed blue line).
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