Effects of temperature on the nitric oxide-dependent modulation of the Frank–Starling mechanism: the fish heart as a case study

Abstract

The Frank–Starling law is a fundamental property of the vertebrate myocardium which allows, when the end-diastolic volume increases, that the consequent stretch of the myocardial fibers generates a more forceful contraction. It has been shown that 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). With the use of isolated working heart preparations, this study investigated 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. Together, these data suggest that the NO synthase/NO-dependent modulation of the Frank–Starling mechanism in fish is sensitive to thermal stress.