Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle
| Autor: | Tsuyoshi Shinozaki, J. L. Wilkens, T. Yazawa, H. E. D. J. Ter Keurs |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
medicine.medical_specialty
Nifedipine Physiology Sarcoplasm Aquatic Science Proctolin Fluorescence Membrane Potentials Caffeine Internal medicine medicine Animals Molecular Biology Ecology Evolution Behavior and Systematics Sarcolemma Voltage-dependent calcium channel Ryanodine Ryanodine receptor Chemistry Myocardium Neuropeptides Cardiac muscle Calcium Channel Blockers musculoskeletal system Myocardial Contraction Nephropidae Sarcoplasmic Reticulum medicine.anatomical_structure Endocrinology Verapamil Insect Science Anesthesia Calcium Animal Science and Zoology Calcium Channels Contracture medicine.symptom Microelectrodes Oligopeptides Cadmium medicine.drug |
| Zdroj: | Journal of Experimental Biology. 208:737-747 |
| ISSN: | 1477-9145 0022-0949 |
| DOI: | 10.1242/jeb.01430 |
| Popis: | SUMMARYAt the threshold concentration (1-10 pmol l-1), the neuropeptide hormones proctolin (PR) and the FLRFamide-like peptide (FLP) F2cause 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. |
| Databáze: | OpenAIRE |
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