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.