The effects of thermal changes on the nitric oxide-dependent modulation of the Frank–Starling mechanism: The eel heart as a paradigm

A fundamental property of vertebrate myocardium is the Frank–Starling mechanism which allows, when the end-diastolic volume increases, that the consequent stretch of the myocardial fibres generates a more forceful contraction. In the eel (Anguilla anguilla) heart, nitric oxide (NO) exerts a direct myocardial relaxant effect, increasing the sensitivity of the Frank–Starling response (Garofalo et al., 2009). Using isolated working heart preparations, this study examined the relationship between NO modulation of Frank–Starling response and temperature challenges in the eel. The results showed that, while in long-term acclimated fish (spring animals perfused at 20°C and winter animals perfused at 10°C) the inhibition of NO production by L-N5 (1-iminoethyl)ornithine (L-NIO) significantly reduced the Frank–Starling response, under thermal shock conditions (spring animals perfused at 10 or 15°C and winter animals perfused at 15 or 20°C) L-NIO treatment resulted without effect. Western blotting analysis revealed a decrease of peNOS and pAkt expressions in samples subjected to thermal shock. Moreover, an increase in Hsp90 protein levels was observed under heat thermal stress. These data suggest that in fish the NO synthase/NO-dependent modulation of the Frank–Starling mechanism is sensitive to thermal stress