scholarly journals Calphostin C, a Potent and Specific Inhibitor of Protein Kinase C, Reduces Phorbol Ester-Induced but Not Primary Ca2+-Induced Catecholamine Secretion from Digitonin-Permeabilized Bovine Adrenal Medullary Cells

1994 ◽  
Vol 64 (3) ◽  
pp. 217-220 ◽  
Author(s):  
Minoru Isosaki ◽  
Naoki Minami ◽  
Toshikatsu Nakashima
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Specific Inhibitor ◽  
Catecholamine Secretion ◽  
Calphostin C ◽  
Kinase C ◽  
Adrenal Medullary Cells ◽  
Medullary Cells

Does protein kinase C play a role in ischemic preconditioning in rat hearts?

1995 ◽  
Vol 268 (1) ◽  
pp. H426-H431 ◽  
Author(s):  
Y. Li ◽  
R. A. Kloner
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Specific Inhibitor ◽  
Myocardial Infarct Size ◽  
Calphostin C ◽  
Kinase C

Protein kinase C (PKC) has been implicated in the cardioprotective effects of ischemic preconditioning in rabbits, but whether it plays a role in rats is unknown. We tested this preconditioning PKC theory by assessing whether the inhibition of PKC with calphostin C, a potent and specific inhibitor of PKC, can block the preconditioning effects in this model. Four groups of rats were studied: 1) control + vehicle, 2) control + calphostin C, 3) preconditioning + vehicle, and 4) preconditioning + calphostin C. All rats underwent 90 min of coronary occlusion followed by 4 h of reperfusion; in addition, preconditioned rats underwent three 3-min episodes of ischemia and 5 min of reperfusion before the 90 min of ischemia. Two injections of vehicle or calphostin C (0.1 mg/kg) were administered in intravenous boluses 29 min and 3 min before the 90-min coronary occlusion, i.e., one dose was given 5 min before preconditioning, and another dose was given between preconditioning and the sustained 90 min of ischemia in preconditioned rats. After 4 h of reperfusion, the area at risk (AR) was delineated by dye injection and area of necrosis was assessed by triphenyltetrazolium chloride staining. The electrocardiogram was recorded for the incidence of ventricular tachycardia (VT) and ventricular fibrillation. AR was similar in all four groups. In the nonpreconditioned control rats receiving vehicle, myocardial infarct size expressed as a percentage of the AR averaged 45.7 +/- 1.7%. Pretreatment with calphostin C had no effect on infarct size (48.9 +/- 3.4%) in nonpreconditioned control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Veratridine causes the Ca2+-dependent increase in diacylglycerol formation and translocation of protein kinase C to membranes in cultured bovine adrenal medullary cells

1992 ◽  
Vol 346 (1) ◽  
pp. 76-81 ◽  
Author(s):  
Yasuhito Uezono ◽  
Akihiko Wada ◽  
Nobuyuki Yanagihara ◽  
Hideyuki Kobayashi ◽  
Tsunetaka Mizuki ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase C ◽  
Adrenal Medullary Cells ◽  
Medullary Cells
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