title: Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle.
abstract: At the threshold concentration (1-10 pmol l(-1)), the neuropeptide hormones proctolin (PR) and the FLRFamide-like peptide (FLP) F(2) cause an increase in amplitude of electrically evoked contractions (each contraction is a brief tetanus) of lobster heart ostial muscle. At higher concentrations each peptide also induces an increase in tonus (contracture). The PR-induced contracture and augmentation of tetani are proportional to increases in [Ca2+]i. The rate of onset and recovery of peptide-induced effects on both tetani and contracture appeared to reduced by Ca2+ storage by the sarcoplasmic reticulum (SR). Enhanced tetani following a contracture may be due to enhanced voltage-gated Ca2+ current and sarcoplasmic reticular (SR) Ca2+ loading. The SR Ca2+ loading appears to be specific for PR and F2, since glutamic-acid-induced contractures are not followed by increased tetani. The prolonged elevation of [Ca2+]i during contracture causes a right-ward shift in the force-pCa curve indicating a decrease in myofibrillar sensitivity to Ca2+. Blocking voltage-gated Ca2+ channels with Cd2+, nifedipine or verapamil, while reducing tetani, does not prevent peptide-induced contracture and enhanced tetani. Opening SR Ca2+ channels and depleting SR Ca2+ with either caffeine or ryanodine blocked tetani but permitted accelerated peptide-induced contractures. We conclude that PR and F2 at low concentration enhance voltage-dependent Ca2+ induced Ca2+ release from the SR, while higher hormone levels directly gate Ca2+ entry across the sarcolemma.
authors.affiliation: Department of Biological Sciences, University of Calgary, Calgary, Canada. wilkens@ucalgary.ca
authors.forename: J L
authors.initials: JL
authors.lastname: Wilkens
authors.forename: T
authors.initials: T
authors.lastname: Shinozaki
authors.forename: T
authors.initials: T
authors.lastname: Yazawa
authors.forename: H E D J
authors.initials: HE
authors.lastname: ter Keurs
mesh_terms: D000818:Animals; D002104:Cadmium / Q000378:metabolism; D002110:Caffeine / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D005453:Fluorescence; D008564:Membrane Potentials; D008839:Microelectrodes; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D008121:Nephropidae / Q000378:metabolism*; D009479:Neuropeptides / Q000378:metabolism* / Q000494:pharmacology; D009543:Nifedipine / Q000378:metabolism; D009842:Oligopeptides / Q000378:metabolism* / Q000494:pharmacology; D012433:Ryanodine / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D014700:Verapamil / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009479:Neuropeptides; D009842:Oligopeptides; D002104:Cadmium; D012433:Ryanodine; D002110:Caffeine; C011536:proctolin; C066148:phenylalanyl-leucyl-arginyl phenylalaninamide; D014700:Verapamil; D009543:Nifedipine; D002118:Calcium