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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

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

J. L. Wilkens^1,*, T. Shinozaki², T. Yazawa³ and H. E. D. J. ter Keurs⁴

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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