Porphyrin induced calcium release from skeletal muscle sarcoplasmic reticulum

• Published in: Archives of biochemistry and biophysics Vol. 301; no. 2; p. 396
• Main Authors: Abramson, J J, Milne, S, Buck, E, Pessah, I N
• Format: Journal Article
• Language: English
• Published: United States 01-03-1993
• Subjects: Adenosine Triphosphate - analogs & derivatives; Adenosine Triphosphate - pharmacology; Animals; Caffeine - pharmacology; Calcium - metabolism; Calcium Channels - drug effects; Calcium Channels - metabolism; Dithiothreitol - pharmacology; Magnesium - pharmacology; Mesoporphyrins - pharmacology; Porphyrins - pharmacology; Rabbits; Ruthenium Red - pharmacology; Ryanodine - metabolism; Sarcoplasmic Reticulum - drug effects; Sarcoplasmic Reticulum - metabolism
• ISSN: 0003-9861
• DOI: 10.1006/abbi.1993.1162

Micromolar concentrations of the porphyrin mesotetra(4-N-methylpyridyl)porphine tetraiodide is shown to induce rapid release of Ca2+ from skeletal muscle sarcoplasmic reticulum vesicles. Porphyrin-induced Ca2+ release is stimulated by ATP (KdATP = 100 microM) and Ca2+ (KdCa = 1 microM) and is inhibited by Mg2+ (KI = 220 microM) and ruthenium red (KI = 7 nM). The porphyrin is also shown to stimulate high affinity [3H]ryanodine binding by decreasing the dissociation constant (kd) and increasing the binding capacity (Bmax). Moreover, in the presence of Mg2+, receptor binding is sensitized to activation by Ca2+, and porphyrin-stimulated channel activity is sensitized to activation by Ca2+. These observations show that porphyrin-induced Ca2+ release is due to a direct interaction with the Ca2+ release protein from sarcoplasmic reticulum.