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First published online February 4, 2005
Journal of Experimental Biology 208, 737-747 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01430
Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle
1 Department of Biological Sciences, University of Calgary, Calgary,
Canada
2 Department of Cardiovascular Medicine, Tohoku Graduate School of Medical
Sciences, Sendai, Japan
3 Department of Biology, Tokyo Metropolitan University, Minamiohsawa 1-1,
Hachioji, Japan
4 Faculty of Medicine, University of Calgary, Calgary, Canada
* Author for correspondence (e-mail: wilkens{at}ucalgary.ca)
Accepted 6 December 2004
At the threshold concentration (1-10 pmol l-1), the neuropeptide hormones proctolin (PR) and the FLRFamide-like peptide (FLP) F2 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.
Key words: F2, proctolin, calcium, cardiac muscle, lobster
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