scholarly journals A kinetic model of beta-adrenergic control in cardiac myocytes

Physiome ◽  
2021 ◽  
Author(s):  
Shelley Fong ◽  
Jeffrey J. Saucerman

The system of equations and figures presented in Saucerman et al. (2003) are verified and reproduced in this paper's curation effort. These checks are performed in MATLAB. With some parameter additions and modifications, we can reproduce all figures with small mismatches.

Physiome ◽  
2021 ◽  
Author(s):  
Shelley Fong ◽  
Jeffrey J. Saucerman

The system of equations and figures presented in Saucerman et al. (2003) are verified and reproduced in this paper's curation effort. These checks are performed in MATLAB. With some parameter additions and modifications, we can reproduce all figures with small mismatches.


1992 ◽  
Vol 71 (4) ◽  
pp. 870-882 ◽  
Author(s):  
G Gambassi ◽  
H A Spurgeon ◽  
E G Lakatta ◽  
P S Blank ◽  
M C Capogrossi

Nephron ◽  
1986 ◽  
Vol 43 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Margaret Johnson Bia ◽  
David Lu ◽  
Karen Tyler ◽  
Ralph A. De Fronzo

1994 ◽  
Vol 267 (5) ◽  
pp. H1753-H1758 ◽  
Author(s):  
G. J. Rozanski ◽  
R. C. Witt

Modulation of the beta-adrenergic control of cardiac L-type Ca2+ current (Ica) by human recombinant interleukin-1 beta (IL-1) was examined in adult guinea pig ventricular myocytes using the whole cell voltage-clamp technique. ICa was elicited in Cs(+)-loaded myocytes by depolarizing pulses from a holding potential of -40 mV. Isoproterenol (0.01 and 1 microM) exposed to myocytes pretreated with 1 ng/ml IL-1 evoked a significantly smaller increase in ICa density compared with control cells. This IL-1-mediated decrease in beta-responsiveness was usually observed with pretreatment periods of > 1 h and varied as a function of the L-arginine concentration of the pretreatment medium. In addition, it was prevented by 1) IL-1 receptor antagonist, 2) substituting D-arginine for L-arginine, or 3) incubating cells with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. Thus the present data illustrate that IL-1 significantly alters the beta-adrenergic control of cardiac Ca2+ channels by cellular mechanisms that involve the activation of nitric oxide synthase. These mechanisms may play a role in altering ventricular function during cytokine-mediated inflammatory processes affecting the heart.


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