scholarly journals INHIBITORY EFFECT OF ^|^beta;-HYDROXYBUTYRIC ACID ON L-TYPE Ca2+ CURRENT UNDER ^|^beta;-ADRENERGIC STIMULATION IN GUINEA PIG CARDIAC VENTRICULAR MYOCYTES

2012 ◽  
Vol 58 (2) ◽  
pp. 144-150 ◽  
Author(s):  
MASATO KURIHARA ◽  
YOUICHI AKAMA ◽  
JUNKO KIMURA
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Hydroxybutyric Acid ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory effect of aprindine on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2002 ◽  
Vol 136 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Munekazu Shigekawa ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory Effect of Cibenzoline on Na+/Ca2+ Exchange Current in Guinea-Pig Cardiac Ventricular Myocytes

2012 ◽  
Vol 120 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Tomomi Yamakawa ◽  
Yasuhide Watanabe ◽  
Hiroshi Watanabe ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory effect of 2,3-butanedione monoxime (BDM) on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2001 ◽  
Vol 132 (6) ◽  
pp. 1317-1325 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Isao Matsuoka ◽  
Satoko Ohkubo ◽  
Tomoyuki Ono ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Butanedione Monoxime ◽  
Cardiac Ventricular Myocytes

Effects of epinephrine on insulin-stimulated glucose uptake and GLUT-4 phosphorylation in muscle

1997 ◽  
Vol 273 (3) ◽  
pp. C1082-C1087 ◽  
Author(s):  
A. D. Lee ◽  
P. A. Hansen ◽  
J. Schluter ◽  
E. A. Gulve ◽  
J. Gao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Inhibitory Effect ◽  
Phosphate Concentration ◽  
Intrinsic Activity ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Glut 4

beta-Adrenergic stimulation has been reported to inhibit insulin-stimulated glucose transport in adipocytes. This effect has been attributed to a decrease in the intrinsic activity of the GLUT-4 isoform of the glucose transporter that is mediated by phosphorylation of GLUT-4. Early studies showed no inhibition of insulin-stimulated glucose transport by epinephrine in skeletal muscle. The purpose of this study was to determine the effect of epinephrine on GLUT-4 phosphorylation, and reevaluate the effect of beta-adrenergic stimulation on insulin-activated glucose transport, in skeletal muscle. We found that 1 microM epinephrine, which raised adenosine 3',5'-cyclic monophosphate approximately ninefold, resulted in GLUT-4 phosphorylation in rat skeletal muscle but had no inhibitory effect on insulin-stimulated 3-O-methyl-D-glucose (3-MG) transport. In contrast to 3-MG transport, the uptakes of 2-deoxyglucose and glucose were markedly inhibited by epinephrine treatment. This inhibitory effect was presumably mediated by stimulation of glycogenolysis, which resulted in an increase in glucose 6-phosphate concentration to levels known to severely inhibit hexokinase. We conclude that 1) beta-adrenergic stimulation decreases glucose uptake by raising glucose 6-phosphate concentration, thus inhibiting hexokinase, but does not inhibit insulin-stimulated glucose transport and 2) phosphorylation of GLUT-4 has no effect on glucose transport in skeletal muscle.

Troponin I phosphorylation in spontaneously hypertensive rat heart: effect of beta-adrenergic stimulation

1997 ◽  
Vol 273 (3) ◽  
pp. H1440-H1451 ◽  
Author(s):  
B. K. McConnell ◽  
C. S. Moravec ◽  
I. Morano ◽  
M. Bond
Keyword(s):  
Troponin I ◽  
Ventricular Myocytes ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Spontaneously Hypertensive ◽  
Myosin Light Chain 2 ◽  
Wistar Kyoto ◽  
Phospholamban Phosphorylation

We compared baseline and protein kinase A (PKA)-dependent troponin I (TnI) phosphorylation in 32Pi-labeled left ventricular myocytes from hearts of 26-wk spontaneously hypertensive rats (SHR) and Wistar-Kyoto controls (WKY). TnI phosphorylation was normalized to myosin light chain 2 phosphorylation, which was invariant. There was no difference in baseline TnI phosphorylation in SHR and WKY, but stimulation with isoproterenol, norepinephrine plus prazosin, forskolin, chloroadenosine 3',5'-cyclic monophosphate, or 3-isobutyl-1-methylxanthine caused a greater increase in TnI phosphorylation in the SHR than in the WKY. This was observed both in the presence and absence of the phosphatase inhibitor calyculin A; thus the differences in TnI phosphorylation between SHR and WKY are not due to decreased phosphatase activity in the SHR. After stimulation of the beta-adrenergic pathway, phospholamban phosphorylation was not different in SHR and WKY, indicating that the observed differences may be specific for PKA phosphorylation of TnI. The increased PKA-dependent TnI phosphorylation in the SHR resulted in decreased Ca2+ sensitivity of actomyosin adenosinetriphosphatase activity as compared with the WKY. We conclude that increased PKA-dependent TnI phosphorylation in the SHR may contribute to the impaired response to sympathetic stimulation.

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