Abstract
The mechanisms of cAMP action on the contractility of the isolated heart were studied in the snail Helix pomatia. Serotonin is a powerful activator of heart contractility in this animal. Preincubation of the isolated heart ventricle with the activator of protein kinase A (PKA) Sp-8-bromoadenosine-3',5'-cyclic monophosphothioate (200 microM) or the activator of Epac proteins 8-(4-chlorophenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate (100 microM) proved to enhance the amplitude of contractions induced by serotonin. Two types of changes in the contractile response were observed: each agent caused either a uniform increase in the amplitude of heart contractions at all concentrations of serotonin or an abrupt increase in the response to the first minimum dose of serotonin. These results indicate that Epac proteins along with PKA are involved in the transmission of cAMP effect on heart contractility.
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