Comparative Anti-Ischemic Effects of Dihydropyridine Calcium Antagonists in Isolated Perfused Rat Hearts: Relationship of Cardiodepression and Cardioprotection

Pharmacology ◽  
1990 ◽  
Vol 40 (3) ◽  
pp. 137-149 ◽  
Author(s):  
Gary J. Grover ◽  
Steven Dzwonczyk ◽  
Paul G. Sleph
Keyword(s):  
Calcium Antagonists ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Relationship Of ◽  
Isolated Perfused Rat Hearts

Chaotic Heart Rate Dynamics in Isolated Perfused Rat Hearts

1989 ◽  
pp. 215-224 ◽  
Author(s):  
Joseph P. Zbilut ◽  
Gottfried Mayer-Kress ◽  
Paul A. Sobotka ◽  
Michael O’Toole ◽  
John X. Thomas
Keyword(s):  
Heart Rate ◽  
Rat Hearts ◽  
Heart Rate Dynamics ◽  
Perfused Rat Hearts ◽  
Isolated Perfused Rat Hearts

Glucocorticoid receptor activation in isolated perfused rat hearts

1989 ◽  
Vol 256 (2) ◽  
pp. C219-C225 ◽  
Author(s):  
S. M. Czerwinski ◽  
E. E. McKee ◽  
R. C. Hickson
Keyword(s):  
Glucocorticoid Receptor ◽  
Triamcinolone Acetonide ◽  
Deae Cellulose ◽  
Potassium Phosphate ◽  
Receptor Activation ◽  
Receptor Complexes ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Cellulose Binding ◽  
Isolated Perfused Rat Hearts

The formation of unactivated and activated glucocorticoid receptor complexes was studied in intact, isolated, perfused rat hearts in the presence of [3H]triamcinolone acetonide. Receptor activation, as quantified by the DNA-cellulose-binding assay, began to increase within 30 s of perfusion and reached a final steady-state level (t 1/2 = 4.6 min) with 46% of the steroid-receptor complexes bound to DNA-cellulose. With the use of a linear potassium phosphate (KP) gradient (5-400 mM), unactivated receptors eluted from DEAE-cellulose anion exchange columns at approximately 250 mM KP. Two activated receptor forms appeared, which eluted either in the wash fraction (binder IB) or between 50 and 100 mM KP (binder II) and occurred with half times of 1.3 and 2.7 min, respectively. Postperfusion cytosol preparation did not markedly influence the results as receptor binding was reduced by 10% or less when a 100-fold excess of unlabeled triamcinolone acetonide was included in the homogenizing buffer. We conclude from these results that glucocorticoids are able to exert a direct effect on the heart through binding to their own receptor in the absence of endogenous hormones. The time dependency of receptor activation supports a physiological role for this process. However, activation rates, determined from conformational changes associated with altered DEAE-cellulose elution profiles and appearance of activated receptor forms, occur earlier and may not be coordinated with the rate of activation as quantified by DNA-cellulose binding.

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