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

• Published in: Journal of experimental biology Vol. 208; no. Pt 4; pp. 737 - 747
• Main Authors: Wilkens, J L, Shinozaki, T, Yazawa, T, ter Keurs, H E D J
• Format: Journal Article
• Language: English
• Published: England 01.02.2005
• Subjects: Animals; Cadmium - metabolism; Caffeine - metabolism; Calcium - metabolism; Calcium Channel Blockers - metabolism; Calcium Channels - metabolism; Clostridium tetani; Fluorescence; Homarus americanus; Marine; Membrane Potentials; Microelectrodes; Myocardial Contraction - drug effects; Myocardium - metabolism; Nephropidae - metabolism; Neuropeptides - metabolism; Neuropeptides - pharmacology; Nifedipine - metabolism; Oligopeptides - metabolism; Oligopeptides - pharmacology; Ryanodine - metabolism; Sarcoplasmic Reticulum - drug effects; Sarcoplasmic Reticulum - metabolism; Verapamil - metabolism
• ISSN: 0022-0949; 1477-9145
• DOI: 10.1242/jeb.01430

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.