Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle

摘要

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 [Ca(2+)](i). The rate of onset and recovery of peptide-induced effects on both tetani and contracture appeared to reduced by Ca(2+) storage by the sarcoplasmic reticulum (SR). Enhanced tetani following a contracture may be due to enhanced voltage-gated Ca(2+) current and sarcoplasmic reticular (SR) Ca(2+) loading. The SR Ca(2+) loading appears to be specific for PR and F(2), since glutamic-acid-induced contractures are not followed by increased tetani. The prolonged elevation of [Ca(2+)](i) during contracture causes a right-ward shift in the force-pCa curve indicating a decrease in myofibrillar sensitivity to Ca(2+). Blocking voltage-gated Ca(2+) channels with Cd(2+), nifedipine or verapamil, while reducing tetani, does not prevent peptide-induced contracture and enhanced tetani. Opening SR Ca(2+) channels and depleting SR Ca(2+) with either caffeine or ryanodine blocked tetani but permitted accelerated peptide-induced contractures. We conclude that PR and F(2) at low concentration enhance voltage-dependent Ca(2+) induced Ca(2+) release from the SR, while higher hormone levels directly gate Ca(2+) entry across the sarcolemma.