| Research Abstract |
We studied the effects, on the A.aniculus heart, of a crustacean pericardial peptide, proctolin. Those effects were investigated by means of recording contractile force, intracellular membrane potential of the myocardium and extracellular potential from cardiac ganglionic cells. We used semi-intact hearts, isolated together with the dorsal, carapace, as well as totally isolated hearts. Threshold concentrations for positively inotropic and positively tonotropic effects were approximately 10^<-13> M and 10^<-10> M, respectively. At 10^<-7> M, inotropic effects amounted to more than 150% of the normal beat amplitude. Initially positive chronotropic effects were followed by negative effects during a period of perfusion with proctolin (10^<-6> M - 10^<-5> M). The inotropic effects resulted mainly from augmentation of the intra-burst impulse rate of cardiac ganglionic cells. The positively chronotropic effects (<50%) reflected increases in burst rate of the ganglion. The amplitude of the compound EJPs and that of the muscle action potentials were augmented, while conductance of the myocardial cell membrane was not changed, during proctolin application. Positively tonotropic effects were observed as contracture even in TTX-containing saline. The contracture was abolished in saline containing a protein kinase inhibitor, H-7. H-7 did not affect myocardial membrane potential but slightly enhanced ganglionic activity. An adenylate cyclase activator, forskolin, and a G-protein activator, cholera toxin, enhanced ganglionic activity but not contracture. In the presence of A1F_4^-, proctolin effects were not augmented. Certain phosphodiesterase inhibitors, caffeine, theophylline, 3-methylxanthine and IBMX affected the ganglion but not myocardial activity itself. That is, in the presence of the inhibitors, proctolin actions on the cardiac ganglion, but not on the myocardial cells, were significantly augmented. Not dibutyryl cGMP, but instead
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