TY - JOUR

T1 - Excitation evoked by FMRFamide and FLRFamide in the heart of Buccinum undatum and evidence for inositol 1,4,5-trisphosphate as an RF-tetrapeptide second messenger.

AU - Ellis, A. M.

AU - Huddart, H.

PY - 2000/9

Y1 - 2000/9

N2 - In this study the relative potencies of four established molluscan cardioexcitatory agents were examined on Buccinum heart. The potencies were, in decending order: phenylalanine-leucine-arginine-phenylalanine-NH2 (FLRFamide) > phenylalanine-methionine-arginine-phenylalanine-NH2 (FMRFamide; 80% of maximum) > 5-hydroxytryptamine (5HT; 60% of maximum) > guanosine triphosphate (GTP; 15% of maximum). FMRFamide and FLRFamide had similar dose-response curve patterns with thresholds at 10−9 mol l−1 but FLRFamide was more potent than FMRFamide. The superfused atrium was much less sensitive to all agonists than the internally perfused ventricle. FLRFamide and FMRFamide induced small depolarizations (1–2 mV) which triggered a burst of action potentials of about 5 mV which on reaching 4 mV triggered a burst of fast twitch contractions. Lithium, at high concentrations inhibited FMRFamide and 5-HT responses of internally perfused ventricles. Neomycin also inhibited peptide responses, but was without effect on 5-HT responses. Heparin, however, for technical reasons was without effect on ventricular responses to all three agonists. FMRFamide and FLRFamide appear to share a common receptor, the potency difference being due to the substitution of leucine for methionine in FLRFamide. The RF N-terminal sequence appears crucial for receptor activation. The Phospholipase C inhibitor neomycin equally inhibits responses to the two peptides while 5-HT responses are unaffected. This implicates a peptide/receptor interaction which activated inositol 1,4,5-trisphosphate (IP3) as a second messenger.

AB - In this study the relative potencies of four established molluscan cardioexcitatory agents were examined on Buccinum heart. The potencies were, in decending order: phenylalanine-leucine-arginine-phenylalanine-NH2 (FLRFamide) > phenylalanine-methionine-arginine-phenylalanine-NH2 (FMRFamide; 80% of maximum) > 5-hydroxytryptamine (5HT; 60% of maximum) > guanosine triphosphate (GTP; 15% of maximum). FMRFamide and FLRFamide had similar dose-response curve patterns with thresholds at 10−9 mol l−1 but FLRFamide was more potent than FMRFamide. The superfused atrium was much less sensitive to all agonists than the internally perfused ventricle. FLRFamide and FMRFamide induced small depolarizations (1–2 mV) which triggered a burst of action potentials of about 5 mV which on reaching 4 mV triggered a burst of fast twitch contractions. Lithium, at high concentrations inhibited FMRFamide and 5-HT responses of internally perfused ventricles. Neomycin also inhibited peptide responses, but was without effect on 5-HT responses. Heparin, however, for technical reasons was without effect on ventricular responses to all three agonists. FMRFamide and FLRFamide appear to share a common receptor, the potency difference being due to the substitution of leucine for methionine in FLRFamide. The RF N-terminal sequence appears crucial for receptor activation. The Phospholipase C inhibitor neomycin equally inhibits responses to the two peptides while 5-HT responses are unaffected. This implicates a peptide/receptor interaction which activated inositol 1,4,5-trisphosphate (IP3) as a second messenger.

KW - Atrium - Buccinum undatum - FLRFamide - FMRFamide - Perfused ventricle

U2 - 10.1007/s003600000110

DO - 10.1007/s003600000110

M3 - Journal article

VL - 170

SP - 351

EP - 356

JO - Journal of Comparative Physiology B

JF - Journal of Comparative Physiology B

SN - 0174-1578

IS - 5-6

ER -