A possible physiological role of the Ca-dependent protease calpain and its inhibitor calpastatin on the Ca current in guinea pig myocytes.
The decrease ('run-down') of the L-type Ca2+-current during long-lasting recordings with the whole-cell patch-clamp technique was examined in guinea pig ventricular myocytes. We have tested whether proteolysis is involved in the decay of the Ca2+-current by intracellular application of several concentrations of the Ca2+-dependent proteases calpain I and II, as well as their endogenous inhibitor calpastatin. The major finding was that calpain I and calpain II accelerated the Ca2+-current run-down in a concentration dependent manner, whereas calpastatin retarded it. These observations indicate that a proteolytic degradation of Ca2+-channels might be the reason for the run-down phenomenon.
Belles
B
B
II. Physiologisches Institut, Universität des Saarlandes, Homburg, FRG.
Hescheler
J
J
Trautwein
W
W
Blomgren
K
K
Karlsson
J O
JO
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000302:isolation & purification / Q000502:physiology*; D002154:Calpain / Q000037:antagonists & inhibitors / Q000302:isolation & purification / Q000502:physiology*; D002462:Cell Membrane / Q000378:metabolism; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism
D015220:Calcium Channels; D002135:Calcium-Binding Proteins; C033668:calpastatin; D011493:Protein Kinase C; D002154:Calpain