H2S is as a novel gaseous transmitter that mediates mammalian cardiovascular homeostasis. In non-mammalian vertebrates H2S shows both vasodilatory and vasoconstrictory properties which are species- and vessel-specific. In contrast, its cardiac effects remain almost unexplored. The purpose of the present study was to analyze the effects of H2S on the performance of the avascular heart of Rana esculenta, and to compare them with those obtained on the rat heart, used as mammalian prototype. Attention was focused on the intracellular signaling with particular reference to the interaction with the NO system and S-Sulfhydration of proteins. In the frog heart, NaHS (used as H2S donor, 10-12÷10-7M) dose-dependently decreased inotropism. This effect was reduced by glibenclamide (KATP channels blocker), L-NMMA (NOS inhibitor), ODQ (guanylyl cyclase inhibitor), KT5823 (PKG inhibitor), and it was blocked by Akt1/2 (Akt inhibitor) and by detergent Triton X-100. In the rat, in addition to the classic negative inotropic effect, NaHS (10-12÷10-7M) exhibited negative lusitropism. NaHS treatment induced Akt and eNOS phosphorylation and an increased protein S-sulfhydration that, in the rat heart, includes phospholamban (PLN). Our data suggest that H2S represents a phylogenetically conserved cardioactive molecule. Results obtained on the rat heart extend the role of H2S also to cardiac relaxation. H2S effects involve KATP channels, the Akt/NOS-cGMP/PKG pathway and proteins S-Sulfhydration

Mechanisms of hydrogen sulphide signalling in frog and rat hearts: Akt/eNOS phosphorilation and PLN S-Sulfhydration

Pasqua T;Angelone T.
2013-01-01

Abstract

H2S is as a novel gaseous transmitter that mediates mammalian cardiovascular homeostasis. In non-mammalian vertebrates H2S shows both vasodilatory and vasoconstrictory properties which are species- and vessel-specific. In contrast, its cardiac effects remain almost unexplored. The purpose of the present study was to analyze the effects of H2S on the performance of the avascular heart of Rana esculenta, and to compare them with those obtained on the rat heart, used as mammalian prototype. Attention was focused on the intracellular signaling with particular reference to the interaction with the NO system and S-Sulfhydration of proteins. In the frog heart, NaHS (used as H2S donor, 10-12÷10-7M) dose-dependently decreased inotropism. This effect was reduced by glibenclamide (KATP channels blocker), L-NMMA (NOS inhibitor), ODQ (guanylyl cyclase inhibitor), KT5823 (PKG inhibitor), and it was blocked by Akt1/2 (Akt inhibitor) and by detergent Triton X-100. In the rat, in addition to the classic negative inotropic effect, NaHS (10-12÷10-7M) exhibited negative lusitropism. NaHS treatment induced Akt and eNOS phosphorylation and an increased protein S-sulfhydration that, in the rat heart, includes phospholamban (PLN). Our data suggest that H2S represents a phylogenetically conserved cardioactive molecule. Results obtained on the rat heart extend the role of H2S also to cardiac relaxation. H2S effects involve KATP channels, the Akt/NOS-cGMP/PKG pathway and proteins S-Sulfhydration
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12317/74118
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